(Circulation. 1995;91:2793-2801.)
© 1995 American Heart Association, Inc.
Articles |
Local Delivery of Vascular Endothelial Growth Factor Accelerates Reendothelialization and Attenuates Intimal Hyperplasia in Balloon-Injured Rat Carotid Artery
From the Departments of Medicine (Cardiology) (T.A., C.B., C.P., M.K., S.R., S.B., N.F., J.M.I), Surgery (Cardiovascular) (J.F.S.), and Biomedical Research (T.A., C.B., C.P., M.K., S.R., S.B., N.F., J.M.I.), St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Mass; and the Department of Cardiovascular Research (S.B., N.F.), Genentech, Inc, South San Francisco, Calif.
Correspondence to Jeffrey M. Isner, MD, St Elizabeth's Medical Center, 736 Cambridge St, Boston, MA 02135.
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Abstract |
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Background Most strategies designed to reduce restenosis by the use of pharmacological or biological reagents involve direct inhibition of vascular smooth muscle cell (SMC) proliferation. Alternatively, SMC proliferation might be indirectly inhibited if reendothelialization could be specifically facilitated at sites of balloon-induced arterial injury. Accordingly, we investigated the hypothesis that application of an endothelial cell (EC)-specific mitogen to a freshly denuded intimal surface could accelerate reendothelialization and thereby attenuate intimal hyperplasia.
Methods and Results The left carotid artery of 31 Sprague-Dawley rats was subjected to balloon injury, after which 16 rats were treated with a 30-minute incubation with 100 µg of vascular endothelial growth factor (VEGF), an EC-specific mitogen. Control animals (n=15) received a 30-minute incubation with 0.9% saline. At 2 weeks after balloon injury, carotid artery reendothelialization was markedly superior in the VEGF-treated group compared with the control group (14.59±1.12 versus 7.96±0.51 mm2, P<.0005). The extent of reendothelialization measured at 4 weeks after balloon injury remained superior for arteries treated with VEGF (18.04±0.90 mm2) versus saline (13.42±0.84 mm2, P<.005). Neointimal thickening was correspondingly attenuated to a statistically significant degree in arteries treated with VEGF versus the control group at both the 2-week and 4-week time points. Immunostaining for proliferating cell nuclear antigen (PCNA) disclosed a threefold increase in PCNA-positive cells in the neointima of control arteries versus VEGF-treated arteries at 2 weeks after injury.
Conclusions Application of VEGF, an EC-specific growth regulatory molecule, may be effectively used in vivo to promote reendothelialization and thereby indirectly attenuate neointimal thickening due to SMC proliferation.
Key Words: growth factors • endothelium • neointima • stenosis
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Vascular endothelial growth factor (VEGF) is unique among angiogenic growth factors by virtue of the fact that its high-affinity binding sites (Flt-11 and Flk-1/KDR2 3 ) are present on endothelial cells (ECs) but not on other cell types; consequently, the mitogenic effects of VEGF are limited to ECs.4 5 This contrasts, for example, with acidic and basic fibroblast growth factors (aFGF and bFGF), both of which are mitogenic for smooth muscle cells (SMCs)6 7 and fibroblasts in addition to ECs. Recent studies from our laboratory have documented that VEGF administered as a single intra-arterial bolus of 500 to 1000 µg is sufficiently potent to augment collateral artery development and thereby ameliorate hemodynamic8 and physiological9 deficits in a rabbit model of hindlimb ischemia. The extent to which this is likely related to the potency of VEGF to serve as an EC mitogen is suggested by studies documenting the effects of VEGF on EC proliferation in vitro10 and, more recently, in vivo.11 In the present study, we sought to exploit the EC-specific mitogenic properties of VEGF for another purpose, ie, to expedite reendothelialization of a freshly injured artery. Specifically, we investigated the hypothesis that a single, direct application of VEGF to the intimal surface of a balloon-injured artery could accelerate reendothelialization and reduce neointimal thickening.
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Methods |
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Study Protocol
All surgical procedures were performed by one trained operator. A total of 31 male 2- to 3-month-old Sprague-Dawley rats (weight, 450 to 600 g) were used. All rats were anesthetized with an intraperitoneal injection of pentobarbital sodium solution (60 mg/kg) (Abbott). The method of balloon denudation was adapted from the technique established by Reidy et al.12 The bifurcation of the left common carotid artery was exposed, and blood flow to the site of surgical manipulation was temporarily interrupted by lifting up the left common, internal, and external carotid arteries with surgical ligatures. A 2F Fogarty catheter (Baxter Edwards) was introduced through an arteriotomy in the external carotid artery and advanced to the proximal edge of the omohyoid muscle. To produce deendothelialization injury of the left common carotid artery, we inflated the balloon with saline and withdrew it three times from just under the proximal edge of the omohyoid muscle to the carotid bifurcation. Immediately after removing the balloon catheter, we introduced an infusion cannula into the external carotid artery to administer treatment or control solution into the temporarily isolated segment of left common carotid artery.
The VEGF-treated group of 16 rats received a 30-minute incubation with 100 µg VEGF (Genentech, Inc) in 0.15-mL solution of 0.1% albumin; this solution was shown to contain no detectable lipopolysaccharide. This dosage was arbitrarily selected based in part on previous demonstrations that 500 µg (approximately 1.25 mg/kg) administered as an intra-arterial bolus induced enhanced angiogenesis in a rabbit model of hindlimb ischemia.8 9 The control group of 15 rats received a 30-minute incubation with 0.9% saline solution. After the 30-minute incubation period, which was performed at room temperature, the ligatures applied to the left common and internal carotid arteries were released; the external carotid artery was permanently ligated after the infusion cannula was withdrawn. The choice of agent to be administered was decided in a random manner, and the operator was blinded to the content of treatment solution.
After surgery, the rats were allowed to recuperate, housed in a US Department of Agriculture–approved facility with free access to rat chow (Agway) and water, and exposed to a 12-hour light/dark cycle. The experimental protocol for this project was approved by the St Elizabeth's Medical Center Institutional Animal Care and Use Committee and complied with the "Guide for the Care and Use of Laboratory Animals" (NIH publication No. 86-23, revised 1985).
Rats were killed 2 weeks after injury (2-week VEGF group [n=7], 2-week control group [n=7]) or 4 weeks after injury (4-week VEGF group [n=9], 4-week control group [n=8]).
Necropsy Examination
Thirty minutes before they were killed,
all rats received an
intravenous injection via the tail vein of 0.5 mL 0.5% Evans blue dye
(Sigma Chemical Co)13 to allow us to microscopically
identify the remaining denuded area. With the rats under general
anesthesia with intraperitoneal sodium
pentobarbital solution (60 mg/kg), a cannula inserted into the left
ventricle was used to perfuse phosphate-buffered saline (PBS) in situ
at a pressure of 90 mm Hg until the effluent ran clear via bilateral
jugular venous vents; this was followed by 5 minutes of fixation with
100% methanol. The same anatomic landmarks used to apply the initial
balloon injury were used to identify the arterial segment to be
harvested. Specifically, the initially denuded segment of the left
common carotid artery, from just under the proximal edge of the
omohyoid muscle to the carotid bifurcation, was dissected free and
incised longitudinally. The harvested segment of carotid artery was
pinned to a cork board, fixed in 100% methanol, and photographed with
a dissecting microscope (STEMI SR, Zeiss) in preparation for
planimetric analysis of the reendothelialized area. Tissues were
then fixed by immersion in 100% methanol, embedded on the longitudinal
edge in paraffin, and cut into 5-µm sections onto silane-coated
slides.
Planimetric Analysis of Reendothelialized Arterial Segment
Planimetric analysis of the photograph of the harvested
arterial segment stained with Evans blue dye to identify the remaining
endothelium-denuded site was performed with a
computerized sketching program (MACMEASURE, version 1.9,
National Institute of Mental Health) on a digitizing board
(Summagraphics) by one analyst, who was blinded to the treatment
regimen. The initially denuded area was defined as the total surface
area of the harvested arterial segment. The length of the harvested
segment corresponded to the total length of the injured segment; in
each case, this length was similarly defined proximally by the carotid
bifurcation and distally by the edge of the omohyoid muscle. The
reendothelialized area was defined macroscopically as the area that was
not stained with Evans blue dye.
Evaluation of Intimal Hyperplasia
Because the thickness of
the native media of the artery wall is
variable and reflects the size (diameter) of the rat carotid artery, it
was used to index the area of neointima resulting from
balloon injury.14 Accordingly, neointimal
thickening was assessed in terms of the intima area–to–media area
ratio (I/M) measured from longitudinal sections of hematoxylin and
eosin– or elastic-trichrome–stained arterial sections by one
analyst,
who was blinded to the treatment regimen. The histological sections
were projected onto the digitizing board, and the areas of the intima
and media were measured with the computerized sketching program by a
technician who was blinded to the treatment regimen.
Evaluation of Proliferative Activity in Injured Artery
Proliferative activity in the injured arterial segment harvested
when the rats were killed was evaluated by histochemical analysis
for proliferating cell nuclear antigen (PCNA), as previously
described.15 Endogenous peroxide activity was blocked with
3.0% hydrogen peroxide in PBS. Nonspecific protein binding was blocked
with 10% normal horse serum. Sections were incubated overnight at
4°C with a mouse monoclonal antibody against PCNA (clone PC10,
Signet) at a dilution of 1:40 in 1% bovine serum albumin/PBS. Negative
control sections were incubated with MOPC-21, a purified nonspecific
mouse monoclonal antibody (Sigma). Bound primary antibody was
detected using an avidin-biotin-immunoperoxidase method according to
supplier's guidelines (Elite Avidin-Biotin Detection System, Signet).
Sections were lightly counterstained with hematoxylin. Sections were
finally mounted in aqueous mounting medium. Regenerated
endothelium was identified by immunostaining with
Bandeiraea simplicifolia I lectin (5 µg/mL; Vector
Laboratories). Additional staining for Bandeiraea simplifolia I
lectin B416 was performed on adjacent sections to
identify ECs. For lectin staining, sections pretreated with 0.3%
hydrogen peroxidase were incubated with 5 µg/mL of biotinylated
lectin (Vector) overnight at 4°C. After washing, slides were
incubated with peroxidase-conjugated streptavidin (BioGenex
Laboratories) for 1 hour; 3-amino-9-ethylcarbazole (Signet) was then
applied as a substrate for the enzyme, resulting in a brown reaction
product.
The extent of proliferative activity for each longitudinal section was measured by the number of positive cells in the intima per length in millimeters of the longitudinal section (ie, cells per millimeter). PCNA staining of the rat ileum served as the positive control. Reendothelialized intima was identified as area covered with a lining of cells staining positive for lectin. Nonendothelialized area was defined as an area of intima not covered by a lining of lectin-positive cells. These examinations were performed by one analyst, who was blinded to the treatment regimen.
Scanning Electron Microscopy
Tissue specimens from 4-week
VEGF-treated and 4-week
control animals were studied using scanning electron microscopy to
evaluate the extent of reendothelialization of the harvested arterial
segment. Harvested arteries were fixed overnight at 4°C in 2.5%
glutaraldehyde in 0.13 mol/L cacodylate buffer, pH 7.4. After being
rinsed twice in buffer, specimens were postfixed in 1% ostium
tetroxide at 4°C for 1.5 hours, rinsed three times in cacodylate
buffer, and dehydrated through graded concentrations of ethanol. The
specimens were critical point–dried from 100% ethanol with liquid
CO2. After the specimens were dried, they were bisected to
expose the luminal surface, mounted on stubs, and sputter-coated with
gold. The samples were viewed and photographed at 10 kV with a scanning
electron microscope (model ISI-DS130, International Scientific
Instrument). Photomicrographs were taken at x200 and x700
magnifications.
Statistical Analysis
Results were expressed as
mean±SEM. Differences between groups
were evaluated using two-tailed, unpaired Student's t test.
Differences were considered significant at P<.05.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Total Area of Initial Balloon Injury
Digitized planimetric analysis of the initially deendothelialized area included the total intimal surface area of the balloon-injured carotid artery retrieved when the animals were killed. As indicated, for both treatment and control groups, the length of the excised segment of artery was determined by the identical anatomic landmarks used to direct the initial balloon injury: from just under the proximal edge of the omohyoid muscle, craniad, to the arteriotomy site, caudad. Planimetric analysis disclosed no statistically significant difference between the total area of initial balloon injury (mm2) in the VEGF-treated group (17.6±0.6) and that of the control group (18.3±0.7) (P=NS) (Fig 1
).
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Extent of Reendothelialization
Acceleration of
reendothelialization was observed in the
VEGF-treated group versus the control group at 2 weeks after balloon
injury. The reendothelialized area (in mm2) in the 2-week
control group was 8.0±0.5; in contrast, the reendothelialized area in
the 2-week VEGF-treated group was 14.6±1.1 (P<.0005) (Fig
1
). Representative examples of the macroscopic appearance of
Evans
blue dye–stained segments from control and VEGF-treated animals are
shown in Fig 2. Expressed as a percentage of the total
area that was initially deendothelialized, the reendothelialized area
in the control group was 44.0±3.6%; in contrast, the percentage of
reendothelialized area in the VEGF-treated group was nearly twice as
great (80.7±4.9%) (P<.0001) (Fig 3).
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The extent of reendothelialization measured at 4 weeks after balloon
injury remained superior for arteries treated with VEGF versus arteries
of control animals. The reendothelialized area (in mm2) in
the 4-week control group was 13.4±0.8; in contrast, the
reendothelialized area in the 4-week VEGF-treated group was 18.0±0.9
(P<.005) (Fig 1). Although reendothelialization in
the
control group at 4 weeks extended to only 75.6±6.0% of the total area
of initial balloon injury, reendothelialization at 4 weeks was nearly
complete (94.9±1.7%) among the VEGF-treated group
(P<.005) (Fig 3).
Scanning electron
microscopy disclosed a regular and smooth-surfaced
endothelial lining in the 4-week VEGF group, similar to the endothelial
lining of a normal, uninjured rat carotid artery. The intimal surface
of segments harvested from the 4-week control group, however,
demonstrated an irregular endothelial lining, leaving exposed
subendothelial tissue (Fig 4).
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Neointimal Thickening
A highly significant reduction in
neointimal
thickening was observed in arteries treated with VEGF versus the
control group at both 2 and 4 weeks. For the 2-week control group, I/M
was 1.23±0.07; in contrast, I/M for VEGF-treated balloon-injured
arterial segments was 0.81±0.11 (P<.01) (Figs
5 and 6).
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This difference between the two
groups was more profound at the 4-week
time point. In the control group at 4 weeks, I/M increased further to
1.60±0.12; in contrast, I/M among the arteries treated with VEGF
remained similar at 4 weeks (0.86±0.05) to that measured at 2 weeks
and significantly less than that of the 4-week control group
(P<.0001) (Figs 5 and 6).
Proliferative Activity
Proliferative activity in the
balloon-injured arteries of both
groups was evaluated at 2 weeks and again at 4 weeks. For the 2-week
control group, proliferative activity was significantly higher than
that of the VEGF-treated group. At this time point, proliferative
activity was limited predominantly to the neointima.
PCNA-positive cells were identified more frequently in the
neointima of the 2-week control group (22±4.5
mm-1) than in the neointima of the 2-week
VEGF-treated group (8±3 mm-1) (P<.05) (Fig
7). Furthermore, most of the PCNA-positive cells
identified at this time point were localized to the nonendothelialized
segment of neointima; this was the case for both control
(96.9±1.5%) and VEGF-treated (97.2±2.0%) animals. When analysis
of proliferative activity was limited to the nonendothelialized segment
of neointima, PCNA-positive cells were identified as
frequently in the 2-week VEGF-treated group (36±12
mm-1)
as in the 2-week control group (34±6 mm-1)
(P=NS) (Fig 8). Shown in Fig 9
is a representative illustration of the fact that PCNA-positive
cells were far less frequent in segments of the artery in which the
endothelium had been reestablished than in those in which the
endothelium remained absent; furthermore, Fig 9 shows that
positive
immunostaining for PCNA was commonly observed as well in ECs at
the leading edge of repair.
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At 4 weeks after injury, the frequency of PCNA-positive cells was reduced in both control (0±0 mm-1) and treated (1±1 mm-1) animals, and the difference between these two groups at 4 weeks was insignificant (P=NS). If analysis of proliferative activity at 4 weeks was limited to the nonendothelialized neointima, PCNA-positive cells were as frequent in the narrow zone of residual nonendothelialized neointima of the VEGF-treated group (5±4 mm-1) as in the 4-week control group (5±4 mm-1) (P=NS).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Previous studies carried out in a variety of animal species have repeatedly shown that extensive endothelial denudation of the arterial wall leads to neointimal thickening.17 Because it is difficult to achieve extensive endothelial denudation without injuring the underlying media, it has been difficult to establish with certainty that the loss of endothelial integrity per se constitutes the sole and/or primary basis for neointimal thickening. In fact, in certain animal models, neointimal thickening can be reproducibly created by electrode stimulation18 or other forms of injury19 20 applied exclusively to the adventitial aspect of the vessel wall. Nevertheless, at least four studies13 21 22 23 in the rat model of arterial balloon injury have clearly established an inverse relation between endothelial integrity and SMC proliferation. Moreover, elaboration of extracellular matrix, an important if not dominant contributor to the development of both primary and restenotic lesions in humans,24 is likewise augmented after endothelial disruption.25 26
These experimental studies have been cited to support the notion that certain functions of the endothelium—including barrier regulation of permeability, thrombogenicity, and leukocyte adherence, as well as production of growth-inhibitory molecules—are critical to prevention of luminal narrowing by neointimal thickening.27 This concept has stimulated efforts to preserve intact the endothelium of native veins used for bypass surgery,28 29 accelerate reendothelialization after balloon-induced arterial injury,30 31 and facilitate endothelialization of prosthetic conduits32 33 34 35 or endovascular stents.36 37
In the present study, local delivery of VEGF to the site of balloon injury resulted in expeditious reendothelialization. By 2 weeks after injury, reendothelialization of balloon-injured arterial segments in the VEGF-treated group was 80% complete; this finding represented profound acceleration of repair in comparison to identically injured arteries in the control group, in which reendothelialization remained limited to only 44% of the balloon-injured arterial segment. Even at 4 weeks after injury, natural mechanisms of repair among the control animals failed to match the extent of reendothelialization observed in response to a single application of VEGF: Although reendothelialization was nearly complete in the VEGF-treated group, the injured arterial segment of control animals remained approximately 24% nonendothelialized.
This rapid regeneration of ECs appeared to contribute to suppression of intimal hyperplasia. Animals in the VEGF-treated group showed less intimal thickening than those in the control group at 2 weeks after injury; moreover, the modest extent of neointimal thickening observed among the VEGF-treated animals remained essentially unchanged during the subsequent 2 weeks (weeks 2 to 4 after injury), whereas neointimal thickening in the control group continued to progress. The notion that this observed differential in neointimal thickening truly represents a differential degree of intimal hyperplasia is supported by the results of PCNA immunostaining: The frequency of PCNA-positive cells in the neointima of control animals at 2 weeks was nearly threefold that observed among animals treated with VEGF. The inverse relation between reendothelialization and neointimal SMC proliferation was graphically demonstrated by the fact that >96% of PCNA-positive cells in the neointima of both groups were observed at neointimal sites devoid of endothelium. Neointimal thickening thus developed in association with delayed reendothelialization. Conversely, the observations from this series of animal experiments suggest that if reendothelialization can be accelerated after arterial injury, then associated neointimal thickening may be correspondingly reduced.
In the present study, we did not attempt to measure the extent to which a potential reduction in extracellular matrix may have contributed to reduced intimal thickening in VEGF-treated arteries. This would not be an unexpected finding, given that the inhibitory effect of VEGF on SMC accumulation would likely translate into reduced SMC synthesis of matrix proteoglycans.38 Furthermore, the potential for regenerating ECs to contribute directly via elaboration of mediators capable of matrix degradation cannot be excluded.
The facilitatory effect of VEGF on reendothelialization constitutes a novel therapeutic application for this growth-regulatory molecule. Previous studies from our laboratory established that VEGF administered intra-arterially8 9 or intravenously39 as a single bolus of 500 to 1000 µg was sufficiently potent to accomplish therapeutic angiogenesis in a rabbit model of hindlimb ischemia; more recently, a similarly efficacious effect was demonstrated in a canine40 model of chronic coronary artery occlusion. Both applications—on arterial reendothelialization as well as collateral artery development—derive at least in part from the documented ability of VEGF to stimulate EC proliferation.10 Adjunctive studies using bromodeoxyuridine labeling have quantified the extent to which EC proliferation stimulated by VEGF contributes to the development of collateral vessels in the rabbit hindlimb model.11
Potentially contributory as well, however, and beyond its mitogenic
effects, is the potential for VEGF to modulate qualitative aspects of
EC function.41 Ku et al,42 for example,
demonstrated that direct application of VEGF to isolated segments of
canine coronary arteries induces endothelium-dependent
relaxation. Because the response was diminished by pretreatment with
the tyrosine kinase inhibitor genistein, Ku et al further inferred that
arterial relaxation was in this case mediated by VEGF receptor–induced
tyrosine phosphorylation of phospholipase C-
1. The finding by Peters
et al41 of the fms-like tyrosine kinase
receptor (Flt) in the endothelium of mature (quiescent)
endothelium of adult organs was likewise interpreted as evidence for
the concept that VEGF may be important for the maintenance and repair
of the endothelium.
These quantitative and qualitative effects of VEGF are limited to ECs by virtue of the exclusive disposition of high-affinity binding sites to this cell type. (Interaction of VEGF with lower-affinity binding sites has been shown to induce mononuclear phagocyte chemotaxis.43 44 ) This cell specificity represents a potential advantage of VEGF in contrast to other EC mitogens that have been studied for their ability to promote angiogenesis as well as endothelial repair. In vivo studies performed in the rat carotid artery model of balloon injury, for example, established clear evidence for the mitogenic effect of bFGF on EC replication in vivo and further demonstrated that total EC regrowth could be achieved by administration of bFGF in doses of 12 µg twice weekly for up to 8 weeks.45 In this particular case, concurrent effects on SMC proliferation were not discussed. Previous work from this same group of investigators,46 however, has documented the mitogenic effects of bFGF on SMC proliferation in vivo, including the demonstration that specific antibodies to bFGF inhibit SMC proliferation.47 In the case of aFGF—also a known mitogen for vascular SMCs in vitro48 —low doses (<1% of the doses of bFGF used in the aforementioned studies) administered to this same animal model were shown to have an inhibitory effect on neointimal thickening; although morphometric analyses suggested that the extent of neointimal thickening was inversely related to the extent of reendothelialization, the extent to which endothelial repair per se was completed was not discussed in this report.49
Finally, it is encouraging from a practical standpoint that in the present study, a single application of VEGF was sufficient to facilitate endothelial repair that was 80% complete by 2 weeks after injury. Provided that a similar magnitude of recombinant protein could be efficiently delivered in association with balloon angioplasty, the potential for VEGF to optimize the short-term as well as long-term consequences of this widely used intervention is intriguing. In contrast to most strategies that have been designed to reduce restenosis by directly inhibiting SMC proliferation, the present findings suggest that SMC proliferation might be indirectly inhibited by directly facilitating reendothelialization. In this regard, it will be important to verify that the qualitative characteristics of the neoendothelium demonstrated anatomically in the present study are satisfactory to reestablish those aspects of EC function believed to confer the antithrombotic, antiadhesive, and antiproliferative effects that limit neointimal thickening. Several experimental studies, for example, have suggested that regenerating ECs, particularly soon after disruption, are functionally impaired with regard to vasomotor reactivity of the traumatized vessel.50 51 52 53 Whether the favorable effects of reendothelialization on intimal thickening demonstrated in the present study indicate functional dissociation between effects on vasomotor tone versus SMC proliferation in regenerating ECs remains to be determined.
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Acknowledgments |
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This work was supported in part by Academic Award in Vascular Medicine grant HL-02824 and grant HL-40518, both from the National Heart, Lung, and Blood Institute, National Institutes of Health. Dr Bauters was the recipient of the French Federation of Cardiology Research Fellowship 1993. We gratefully acknowledge Mickey Neely for assistance in the preparation of the manuscript.
Received October 31, 1994; revision received January 18, 1995; accepted January 22, 1995.
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 K. Matsumoto, R. Morishita, A. Moriguchi, N. Tomita, M. Aoki, H. Sakonjo, K. Matsumoto, T. Nakamura, J. Higaki, and T. Ogihara Inhibition of Neointima by Angiotensin-Converting Enzyme Inhibitor in Porcine Coronary Artery Balloon-Injury Model Hypertension, February 1, 2001; 37(2): 270 - 274. [Abstract] [Full Text] [PDF]
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R. Shibata, H. Kai, Y. Seki, S. Kato, M. Morimatsu, K. Kaibuchi, and T. Imaizumi Role of Rho-Associated Kinase in Neointima Formation After Vascular Injury Circulation, January 16, 2001; 103(2): 284 - 289. [Abstract] [Full Text] [PDF]
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H. Morita, H. Kurihara, S. Yoshida, Y. Saito, T. Shindo, Y. Oh-hashi, Y. Kurihara, Y. Yazaki, and R. Nagai Diet-Induced Hyperhomocysteinemia Exacerbates Neointima Formation in Rat Carotid Arteries After Balloon Injury Circulation, January 2, 2001; 103(1): 133 - 139. [Abstract] [Full Text] [PDF]
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 C. Partovian, S. Adnot, B. Raffestin, V. Louzier, M. Levame, I. M. Mavier, P. Lemarchand, and S. Eddahibi Adenovirus-Mediated Lung Vascular Endothelial Growth Factor Overexpression Protects against Hypoxic Pulmonary Hypertension in Rats Am. J. Respir. Cell Mol. Biol., December 1, 2000; 23(6): 762 - 771. [Abstract] [Full Text]
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B. Chandrasekar and J.-F. Tanguay Local delivery of 17-beta-estradiol decreases neointimal hyperplasia after coronary angioplasty in a porcine model J. Am. Coll. Cardiol., November 15, 2000; 36(6): 1972 - 1978. [Abstract] [Full Text] [PDF]
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 S. L. Meyerson, C. L. Skelly, M. A. Curi, and L. B. Schwartz Gene Therapy for Cardiovascular Disease Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 2000; 4(4): 289 - 300. [Abstract] [PDF]
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O. Leppanen, N. Janjic, M.-A. Carlsson, K. Pietras, M. Levin, C. Vargeese, L. S. Green, D. Bergqvist, A. Ostman, and C.-H. Heldin Intimal Hyperplasia Recurs After Removal of PDGF-AB and -BB Inhibition in the Rat Carotid Artery Injury Model Arterioscler. Thromb. Vasc. Biol., November 1, 2000; 20 (11): e89 - e95. [Abstract] [Full Text] [PDF]
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M. O. Hiltunen, M. Laitinen, M. P. Turunen, M. Jeltsch, J. Hartikainen, T. T. Rissanen, J. Laukkanen, M. Niemi, M. Kossila, T. P. Hakkinen, et al. Intravascular Adenovirus-Mediated VEGF-C Gene Transfer Reduces Neointima Formation in Balloon-Denuded Rabbit Aorta Circulation, October 31, 2000; 102(18): 2262 - 2268. [Abstract] [Full Text] [PDF]
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 P.B.J Burton, V.J Owen, S Hafizi, P.J.R Barton, G Carr-White, T Koh, A De Souza, M.H Yacoub, and J.R Pepper Vascular endothelial growth factor release following coronary artery bypass surgery: extracorporeal circulation versus 'beating heart' surgery Eur. Heart J., October 2, 2000; 21(20): 1708 - 1713. [Abstract] [PDF]
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N. Kipshidze, J. J. Ferguson III, M. H. Keelan Jr., H. Sahota, R. Komorowski, L. R. Shankar, P. S. Chawla, C. C. Haudenschild, V. Nikolaychik, and J. W. Moses Endoluminal reconstruction of the arterial wall with endothelial cell/glue matrix reduces restenosis in an atherosclerotic rabbit J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1396 - 1403. [Abstract] [Full Text] [PDF]
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F. D. Kolodgie, A. Farb, and R. Virmani Local Delivery of Ceramide for Restenosis : Is There a Future for Lipid Therapy? Circ. Res., August 18, 2000; 87(4): 264 - 267. [Full Text] [PDF]
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J. Waltenberger, J. Lange, and A. Kranz Vascular Endothelial Growth Factor-A-Induced Chemotaxis of Monocytes Is Attenuated in Patients With Diabetes Mellitus : A Potential Predictor for the Individual Capacity to Develop Collaterals Circulation, July 11, 2000; 102(2): 185 - 190. [Abstract] [Full Text] [PDF]
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I. Zachary, A. Mathur, S. Yla-Herttuala, and J. Martin Vascular Protection : A Novel Nonangiogenic Cardiovascular Role for Vascular Endothelial Growth Factor Arterioscler. Thromb. Vasc. Biol., June 1, 2000; 20(6): 1512 - 1520. [Abstract] [Full Text] [PDF]
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F. Vidal, J. Aragones, A. Alfranca, and M. O. de Landazuri Up-regulation of vascular endothelial growth factor receptor Flt-1 after endothelial denudation: role of transcription factor Egr-1 Blood, June 1, 2000; 95(11): 3387 - 3395. [Abstract] [Full Text] [PDF]
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S. Yasuda, T. Noguchi, M. Gohda, T. Arai, N. Tsutsui, T. Matsuda, and H. Nonogi Single Low-Dose Administration of Human Recombinant Hepatocyte Growth Factor Attenuates Intimal Hyperplasia in a Balloon-Injured Rabbit Iliac Artery Model Circulation, May 30, 2000; 101(21): 2546 - 2549. [Abstract] [Full Text] [PDF]
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H. J. Kwak, S. J. Lee, Y.-H. Lee, C. H. Ryu, K. N. Koh, H. Y. Choi, and G. Y. Koh Angiopoietin-1 Inhibits Irradiation- and Mannitol-Induced Apoptosis in Endothelial Cells Circulation, May 16, 2000; 101(19): 2317 - 2324. [Abstract] [Full Text] [PDF]
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D. Mukherjee, J. Wong, B. Griffin, S. G. Ellis, T. Porter, S. Sen, and J. D. Thomas Ten-fold augmentation of endothelial uptake of vascular endothelial growth factor with ultrasound after systemic administration J. Am. Coll. Cardiol., May 1, 2000; 35(6): 1678 - 1686. [Abstract] [Full Text] [PDF]
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E. R. Schwarz, M. T. Speakman, M. Patterson, S. S. Hale, J. M. Isner, L. H. Kedes, and R. A. Kloner Evaluation of the effects of intramyocardial injection of DNA expressing vascular endothelial growth factor (VEGF) in a myocardial infarction model in the rat--angiogenesis and angioma formation J. Am. Coll. Cardiol., April 1, 2000; 35(5): 1323 - 1330. [Abstract] [Full Text] [PDF]
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K. G. Lehmann, J. J. Popma, J. A. Werner, A. J. Lansky, and R. L. Wilensky Vascular remodeling and the local delivery of cytochalasin B after coronary angioplasty in humans J. Am. Coll. Cardiol., March 1, 2000; 35(3): 583 - 591. [Abstract] [Full Text] [PDF]
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D. Chen, K. Walsh, and J. Wang Regulation of cdk2 Activity in Endothelial Cells That Are Inhibited From Growth by Cell Contact Arterioscler. Thromb. Vasc. Biol., March 1, 2000; 20(3): 629 - 635. [Abstract] [Full Text] [PDF]
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J. Dulak, A. Jozkowicz, A. Dembinska-Kiec, I. Guevara, A. Zdzienicka, D. Zmudzinska-Grochot, I. Florek, A. Wojtowicz, A. Szuba, and J. P. Cooke Nitric Oxide Induces the Synthesis of Vascular Endothelial Growth Factor by Rat Vascular Smooth Muscle Cells Arterioscler. Thromb. Vasc. Biol., March 1, 2000; 20(3): 659 - 666. [Abstract] [Full Text] [PDF]
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 J. Dulak, A. Jozkowicz, A. Ratajska, A. Szuba, J. P Cooke, and A. Dembinska-Kiec Vascular endothelial growth factor is efficiently synthesized in spite of low transfection efficiency of pSG5VEGF plasmids in vascular smooth muscle cells Vascular Medicine, February 1, 2000; 5(1): 33 - 40. [Abstract] [PDF]
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M. O Hiltunen, M. P Turunen, M. Laitinen, and S. Yla-Herttuala Insights into the molecular pathogenesis of atherosclerosis and therapeutic strategies using gene transfer Vascular Medicine, February 1, 2000; 5(1): 41 - 48. [Abstract] [PDF]
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M. F. Flanagan, T. Aoyagi, L. W. Arnold, C. Maute, A. M. Fujii, J. Currier, D. Bergau, H. B. Warren, and K. Rakusan Effects of Chronic Heparin Administration on Coronary Vascular Adaptation to Hypertension and Ventricular Hypertrophy in Sheep Circulation, August 31, 1999; 100(9): 981 - 987. [Abstract] [Full Text] [PDF]
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D. Chen, T. Asahara, K. Krasinski, B. Witzenbichler, J. Yang, M. Magner, M. Kearney, W. A. Frazier, J. M. Isner, and V. Andres Antibody Blockade of Thrombospondin Accelerates Reendothelialization and Reduces Neointima Formation in Balloon-Injured Rat Carotid Artery Circulation, August 24, 1999; 100(8): 849 - 854. [Abstract] [Full Text] [PDF]
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N. Kronemann, A. Bouloumie, S. Bassus, C. M. Kirchmaier, R. Busse, and V. B. Schini-Kerth Aggregating Human Platelets Stimulate Expression of Vascular Endothelial Growth Factor in Cultured Vascular Smooth Muscle Cells Through a Synergistic Effect of Transforming Growth Factor-{beta}1 and Platelet-Derived Growth FactorAB Circulation, August 24, 1999; 100(8): 855 - 860. [Abstract] [Full Text] [PDF]
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J. Y. Jeremy, D. Rowe, A. M. Emsley, and A. C. Newby Nitric oxide and the proliferation of vascular smooth muscle cells Cardiovasc Res, August 15, 1999; 43(3): 580 - 594. [Full Text] [PDF]
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I. Six, E. Van Belle, R. Bordet, D. Corseaux, J. Callebert, B. Dupuis, C. Bauters, and M. E. Bertrand L-Arginine and L-NAME have no effects on the reendothelialization process after arterial balloon injury Cardiovasc Res, August 15, 1999; 43(3): 731 - 738. [Abstract] [Full Text] [PDF]
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M. Harada, Y. Toki, Y. Numaguchi, H. Osanai, T. Ito, K. Okumura, and T. Hayakawa Prostacyclin synthase gene transfer inhibits neointimal formation in rat balloon-injured arteries without bleeding complications Cardiovasc Res, August 1, 1999; 43(2): 481 - 491. [Abstract] [Full Text] [PDF]
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J. M. Isner Cancer and Atherosclerosis : The Broad Mandate of Angiogenesis Circulation, April 6, 1999; 99(13): 1653 - 1655. [Full Text] [PDF]
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 A. Basile-Borgia, J. H Abel, and H. Mahloogi Molecular advances in cardiac and cardiovascular disease Perfusion, March 1, 1999; 14(2): 89 - 99. [Abstract] [PDF]
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M. Camera, P. L. A. Giesen, J. Fallon, B. M. Aufiero, M. Taubman, E. Tremoli, and Y. Nemerson Cooperation Between VEGF and TNF-{alpha} Is Necessary for Exposure of Active Tissue Factor on the Surface of Human Endothelial Cells Arterioscler. Thromb. Vasc. Biol., March 1, 1999; 19(3): 531 - 537. [Abstract] [Full Text] [PDF]
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Y. Numaguchi, K. Naruse, M. Harada, H. Osanai, S. Mokuno, K. Murase, H. Matsui, Y. Toki, T. Ito, K. Okumura, et al. Prostacyclin Synthase Gene Transfer Accelerates Reendothelialization and Inhibits Neointimal Formation in Rat Carotid Arteries After Balloon Injury Arterioscler. Thromb. Vasc. Biol., March 1, 1999; 19(3): 727 - 733. [Abstract] [Full Text] [PDF]
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A. Bouloumie, V. B. Schini-Kerth, and R. Busse Vascular endothelial growth factor up-regulates nitric oxide synthase expression in endothelial cells Cardiovasc Res, March 1, 1999; 41(3): 773 - 780. [Abstract] [Full Text] [PDF]
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Y. Furukawa, A. Matsumori, N. Ohashi, T. Shioi, K. Ono, A. Harada, K. Matsushima, and S. Sasayama Anti–Monocyte Chemoattractant Protein-1/Monocyte Chemotactic and Activating Factor Antibody Inhibits Neointimal Hyperplasia in Injured Rat Carotid Arteries Circ. Res., February 19, 1999; 84(3): 306 - 314. [Abstract] [Full Text] [PDF]
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I. J. Kullo, R. D. Simari, and R. S. Schwartz Vascular Gene Transfer : From Bench to Bedside Arterioscler. Thromb. Vasc. Biol., February 1, 1999; 19(2): 196 - 207. [Full Text] [PDF]
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 C. PUPILLI, L. LASAGNI, P. ROMAGNANI, F. BELLINI, M. MANNELLI, N. MISCIGLIA, C. MAVILIA, U. VELLEI, D. VILLARI, and M. SERIO Angiotensin II Stimulates the Synthesis and Secretion of Vascular Permeability Factor/Vascular Endothelial Growth Factor in Human Mesangial Cells J. Am. Soc. Nephrol., February 1, 1999; 10(2): 245 - 255. [Abstract] [Full Text]
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 G. Neufeld, T. Cohen, S. Gengrinovitch, and Z. Poltorak Vascular endothelial growth factor (VEGF) and its receptors FASEB J, January 1, 1999; 13(1): 9 - 22. [Abstract] [Full Text]
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I. Spyridopoulos, N. Principe, K. L. Krasinski, S.-h. Xu, M. Kearney, M. Magner, J. M. Isner, and D. W. Losordo Restoration of E2F Expression Rescues Vascular Endothelial Cells From Tumor Necrosis Factor-{alpha}–Induced Apoptosis Circulation, December 22, 1998; 98(25): 2883 - 2890. [Abstract] [Full Text] [PDF]
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C. Partovian, S. Adnot, S. Eddahibi, E. Teiger, M. Levame, P. Dreyfus, B. Raffestin, and C. Frelin Heart and lung VEGF mRNA expression in rats with monocrotaline- or hypoxia-induced pulmonary hypertension Am J Physiol Heart Circ Physiol, December 1, 1998; 275(6): H1948 - H1956. [Abstract] [Full Text] [PDF]
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F. Gonzalez-Fernandez, A. Lopez-Farre, J. A. Rodriguez-Feo, J. Farre, J. Guerra, J. Fortes, I. Millas, M. Garcia-Duran, L. Rico, P. Mata, et al. Expression of Inducible Nitric Oxide Synthase After Endothelial Denudation of the Rat Carotid Artery : Role of Platelets Circ. Res., November 30, 1998; 83(11): 1080 - 1087. [Abstract] [Full Text] [PDF]
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H. Wang and J. A. Keiser Vascular Endothelial Growth Factor Upregulates the Expression of Matrix Metalloproteinases in Vascular Smooth Muscle Cells : Role of flt-1 Circ. Res., October 19, 1998; 83(8): 832 - 840. [Abstract] [Full Text] [PDF]
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O. Varenne, S. Pislaru, H. Gillijns, N. Van Pelt, R. D. Gerard, P. Zoldhelyi, F. Van de Werf, D. Collen, and S. P. Janssens Local Adenovirus-Mediated Transfer of Human Endothelial Nitric Oxide Synthase Reduces Luminal Narrowing After Coronary Angioplasty in Pigs Circulation, September 1, 1998; 98(9): 919 - 926. [Abstract] [Full Text] [PDF]
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A. Matsuura, W. Yamochi, K.-i. Hirata, S. Kawashima, and M. Yokoyama Stimulatory Interaction Between Vascular Endothelial Growth Factor and Endothelin-1 on Each Gene Expression Hypertension, July 1, 1998; 32(1): 89 - 95. [Abstract] [Full Text] [PDF]
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M. Oberhoff, S. Novak, C. Herdeg, A. Baumbach, A. Kranzhofer, A. Bohnet, B. Horch, H. Hanke, K. K. Haase, and K. R. Karsch Local and systemic delivery of low molecular weight heparin stimulates the reendothelialization after balloon angioplasty Cardiovasc Res, June 1, 1998; 38(3): 751 - 762. [Abstract] [Full Text] [PDF]
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