(Circulation. 2001;103:2531.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
Modulation of C-Reactive Protein–Mediated Monocyte Chemoattractant Protein-1 Induction in Human Endothelial Cells by Anti-Atherosclerosis Drugs
From the Department of Cardiology (J.C., E.T.H.Y.), University of Texas–MD Anderson Cancer Center; Department of Internal Medicine (V.P., J.T.W., E.T.H.Y.), University of Texas Health Science Center; and the Texas Heart Institute (V.P., J.T.W., E.T.H.Y.), St. Luke’s Episcopal Hospital, Houston, Tex.
Correspondence to Edward T.H. Yeh, MD, Department of Cardiology, 1515 Holcombe Blvd. Box 449, University of Texas–MD Anderson Cancer Center, Houston, TX 77030-4009.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—C-reactive protein (CRP) induces adhesion molecule expression by endothelial cells. However, the effects of CRP on chemokine expression by endothelial cells are not known.
Methods and Results—We
tested the effects of CRP on the production of the chemokines
monocyte chemoattractant protein-1 (MCP-1) and RANTES in
cultured human umbilical vein endothelial cells. The
secretion of chemokines was assessed by ELISA. Incubation with 100
µg/mL recombinant human CRP induced a 7-fold increase in MCP-1 but no
change in RANTES secretion. We showed that the effect of CRP on MCP-1
was present even at 5 µg/mL CRP, with stepwise increases as the
CRP concentration was increased to 10, 50, and 100 µg/mL. The effect
of CRP on MCP-1 induction was not influenced by aspirin (at
concentrations up to 1 mmol/L), but it was significantly inhibited
by 5 µmol/L simvastatin. The peroxisome
proliferator-activated receptor-
activators
fenofibrate (100 µmol/L) and Wy-14649 (100 µmol/L) almost
completely abolished the induction of MCP-1, but the peroxisome
proliferator-activated receptor-
activator
ciglitazone had only a moderate effect.
Conclusions—These results further strengthen the role of CRP in the pathogenesis of vascular inflammation and, likely, atherosclerosis and provide a crucial insight into a novel mechanism of action of anti-atherosclerosis drugs such as simvastatin and fenofibrate.
Key Words: cell adhesion molecules • endothelium • atherosclerosis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Many epidemiological studies have shown that C-reactive protein (CRP) is an important risk factor for atherosclerosis and coronary heart disease.1 The mechanisms underlying this association are not completely clear: although CRP may merely be a nonspecific marker of inflammation, it is possible that CRP plays a direct role in the pathogenesis of inflammation/atherosclerosis. We recently found that CRP directly induces the expression of adhesion molecules by endothelial cells.1 2 3 However, the expression of specific chemokines, particularly monocyte chemoattractant protein-1 (MCP-1), also has a major role in recruiting monocytes into the vessel wall.4 Thus, the aim of the present study was to assess the possible effects of CRP on the expression of chemokines by endothelial cells and to assess the possible role of pharmacological treatment in the modulation of this effect.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Materials
Human umbilical vein endothelial cells (HUVEC; from Cascade) were grown in M199 medium with endothelial cell growth supplement, heparin, and 15% fetal bovine serum. Cells were used at passages 2 to 4.
Recombinant human CRP and highly purified CRP from human
serum were purchased from Calbiochem, and
interleukin-1ß (IL-1ß) was obtained from RandD Systems. All
reagents were endotoxin-free by limulus test (from
Sigma; sensitivity, 0.06 U/mL). Purity of CRP
preparations was also confirmed by SDS-PAGE (single band on silver
staining of overloaded gels). For inhibitory experiments,
HUVEC were pretreated with various peroxisome
proliferator-activated receptor (PPAR)- agonists, including
troglitazone (Parke-Davis), ciglitazone
(Biomol),
15-deoxy-
12,14-prostaglandin
J2 (15d-PGJ2;
Calbiochem); the PPAR agonists fenofibrate
and Wy 14649 (Sigma); the
hydroxymethylglutaryl coenzyme A antagonist
(statin) simvastatin; or vehicle (0.1% DMSO or PBS) at the
concentrations indicated. After 2 hours, the cells were incubated with
CRP or IL-1ß 10 ng/mL for 24 hours. Simvastatin prodrug
(Merck) was activated as previously
described.5
Analysis of Conditioned Medium
Experiments were performed in HUVEC that were
cultured in 12-well plates in medium CS-C with 10 mmol/L HEPES and
15% human serum (Sigma). Culture supernatants
were collected 6 to 24 hours after stimulation with either IL-1ß or
CRP at the concentration indicated. The secretion of MCP-1 and RANTES
was assessed by sandwich ELISA (Quantikine, by RandD Systems). All
determinations were performed in duplicate. Data are expressed as
mean±SD of 5 to 6 separate experiments. Cell viability was assessed by
Trypan blue exclusion.
Analysis of multiple paired data within the same experiments was performed with the nonparametric Friedman test and the Wilcoxon test (GB-STAT V6 software). P<0.05 (2-tailed) was considered significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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CRP Induces Expression of MCP-1 but Not RANTES in HUVEC
In a 24-hour time course study shown in the Figure
(A), CRP at a concentration of 100 µg/mL induced a significant
secretion of MCP-1, with a maximal effect at 24 hours (a 7
fold-increase at 24 hours,
P=0.001). Dose-response
experiments performed with 24-hour incubation showed a significant
induction of MCP-1 even with 5 µg/mL (from 1.1±0.5 ng/mL at baseline
to 2.4±0.9 with 10 µg/mL of CRP) that peaked at 100 µg/mL (up to
9.7±4.8 ng/mL, P=0.001;
Figure,
panel C). The maximal effects of CRP were similar to those observed
after incubation with IL-1ß 10 ng/mL (8.6±3.7 ng/mL,
Figure,
panel B). All these experiments were performed in the presence of 15%
human serum. Incubation with CRP 100 µg/mL did not increase MCP-1
concentrations in HUVEC cultured in serum-free medium
(Figure,
panel C), although the absence of serum did not change the response to
IL-1ß.
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Secretion of RANTES was not increased by incubation with CRP
100 µg/mL
(Figure
,
panel B). Similarly, incubation with IL-1ß 10 ng/mL did not induce
RANTES expression.
Modulation of CRP Effects by Statins and
PPAR Activators
The effects of pretreatment with
simvastatin and several PPAR activators on the
induction of MCP-1 are shown in the
Table.
Simvastatin 5 µmol/L significantly reduced (
43% of
maximal response) the secretion of MCP-1 induced by CRP. Aspirin, even
at high concentrations (up to 1 mmol/L), did not inhibit the
effects of CRP. The PPAR activators troglitazone and
ciglitazone had no significant effects at low concentrations, but they
did significantly inhibit MCP-1 secretion at a high concentration (200
µmol/L ciglitazone). However, 15d-PGJ2 10 µmol/L almost completely
abolished the induction of MCP-1 by CRP. The PPAR
activators fenofibrate (100 µmol/L) and Wy 14649 (100
µmol/L) completely inhibited the secretion of MCP-1, although a lower
concentration (10 µmol/L) of Wy 14649 had no effect.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study shows that CRP induces the expression of MCP-1 but not RANTES in HUVEC. This effect can be modulated by drugs known to inhibit chemokine expression by activated endothelial cells, such as simvastatin and PPAR activators.
CRP is strongly associated with the occurrence of new
cardiovascular events in patients with both
unstable6 and stable angina,
and it is an important risk factor for cardiac mortality in normal
subjects.7 The mechanism(s)
of this association are still unclear. Although CRP can merely be a
marker of an underlying inflammatory/atherosclerotic process, it is
possible that CRP may be directly involved in the pathogenesis of
atherosclerosis/inflammation.1 2 3
CRP can induce the expression of tissue factor by
monocytes,8 9 and
it is present in atherosclerotic plaques but not in the normal
vessel wall.10 CRP deposits
in early atherosclerotic lesions may precede the appearance of
monocytes.11 Recently, we
found that CRP, at concentrations 
5 µg/mL, induces the expression
of the adhesion molecules intracellular adhesion molecule-1 (ICAM-1),
vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in
human endothelial
cells.3 The present study
is the first to demonstrate a direct effect of CRP on the secretion of
a specific chemokine (MCP-1) from endothelial cells.
These effects are evident at CRP concentrations similar to those
observed in patients at an increased risk of new coronary
events12 13 and
are close in magnitude to those observed with the proinflammatory
cytokine IL-1ß. Chemokines, particularly MCP-1, play a key
role in the migration of monocytes and T-cells into the vessel wall and
in the evolution of
atherosclerosis.14 15
Interestingly, neither CRP nor IL-1ß were able to induce
RANTES expression by endothelial cells. In a previous
study, no RANTES was produced after stimulating HUVEC with IL-1ß;
RANTES production was only induced by cotreatment with
interferon-.16
Epidemiological studies have suggested an interaction between CRP and statins17 and aspirin treatment.7 18 Statins may reduce serum CRP levels17 and mortality in patients with low cholesterol levels but high CRP concentrations. Furthermore, statins can inhibit the expression of MCP-1 induced by IL-1 in endothelial cells and monocytes.19 In the present study, treatment with simvastatin partially inhibited the induction of MCP-1 by CRP on endothelial cells.
PPAR activators may reduce the proinflammatory
effects of cytokines on vascular cells and may have beneficial
effects on the progression of atherosclerosis in animal
models.20 21 22 23
Although in a previous study low concentrations of troglitazone (10
µmol/L) inhibited tumor necrosis factor-–induced MCP-1 expression
in endothelial
cells,24 in the present
study, thiazoledinediones had significant effects only at a high
concentration; this concentration was much higher than their affinity
for PPAR, although 15d-PGJ2 had significant effects at
concentrations close to its KD for
PPAR (2.5 µmol/L). However, the inhibitory effects of
15d-PGJ2 may be also due to its inhibition of nuclear factor-
B by
PPAR-independent
mechanisms.25 PPAR
activators, such as fenofibrate and Wy 14649, almost
completely blocked the induction of MCP-1 by CRP. These
anti-inflammatory effects of PPAR activators may be
explained, at least in part, by their inhibition of the nuclear
factor-B and activator protein-1
pathways.26
In conclusion, our study demonstrates that CRP can induce the production of MCP-1 by endothelial cells. These effects can be modulated by pharmacological interventions, particularly simvastatin and fenofibrate. Our findings support the hypothesis of a direct role of CRP in the pathogenesis of inflammation/atherosclerosis and open the way to new pharmacological strategies for its treatment.
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Footnotes |
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Guest Editor for this article was Prediman K. Shah, Cedars-Sinai Medical Center, Los Angeles, Calif.
Received March 30, 2001; revision received April 13, 2001; accepted April 17, 2001.
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 J. Krupinski, M. M. Turu, J. Martinez-Gonzalez, A. Carvajal, J. O. Juan-Babot, E. Iborra, M. Slevin, F. Rubio, and L. Badimon Endogenous Expression of C-Reactive Protein Is Increased in Active (Ulcerated Noncomplicated) Human Carotid Artery Plaques Stroke, May 1, 2006; 37(5): 1200 - 1204. [Abstract] [Full Text] [PDF]
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J.-a Kim, M. Montagnani, K. K. Koh, and M. J. Quon Reciprocal Relationships Between Insulin Resistance and Endothelial Dysfunction: Molecular and Pathophysiological Mechanisms Circulation, April 18, 2006; 113(15): 1888 - 1904. [Abstract] [Full Text] [PDF]
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I. Montero, J. Orbe, N. Varo, O. Beloqui, J. I. Monreal, J. A. Rodriguez, J. Diez, P. Libby, and J. A. Paramo C-Reactive Protein Induces Matrix Metalloproteinase-1 and -10 in Human Endothelial Cells: Implications for Clinical and Subclinical Atherosclerosis J. Am. Coll. Cardiol., April 4, 2006; 47(7): 1369 - 1378. [Abstract] [Full Text] [PDF]
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M. Hermann and F. Ruschitzka Novel anti-inflammatory drugs in hypertension Nephrol. Dial. Transplant., April 1, 2006; 21(4): 859 - 864. [Full Text] [PDF]
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 A. Tedgui and Z. Mallat Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways Physiol Rev, April 1, 2006; 86(2): 515 - 581. [Abstract] [Full Text] [PDF]
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D Skowasch, S Schrempf, C J Preusse, J A Likungu, A Welz, B Luderitz, and G Bauriedel Tissue resident C reactive protein in degenerative aortic valves: correlation with serum C reactive protein concentrations and modification by statins Heart, April 1, 2006; 92(4): 495 - 498. [Abstract] [Full Text] [PDF]
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K. K. Koh, S. H. Han, and M. J. Quon Inflammatory Markers and the Metabolic Syndrome: Insights From Therapeutic Interventions J. Am. Coll. Cardiol., December 6, 2005; 46(11): 1978 - 1985. [Abstract] [Full Text] [PDF]
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 A. E Malavazos, E. Cereda, L. Morricone, C. Coman, M. M Corsi, and B. Ambrosi Monocyte chemoattractant protein 1: a possible link between visceral adipose tissue-associated inflammation and subclinical echocardiographic abnormalities in uncomplicated obesity Eur. J. Endocrinol., December 1, 2005; 153(6): 871 - 877. [Abstract] [Full Text] [PDF]
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 D.-H. Kang, S.-K. Park, I.-K. Lee, and R. J. Johnson Uric Acid-Induced C-Reactive Protein Expression: Implication on Cell Proliferation and Nitric Oxide Production of Human Vascular Cells J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3553 - 3562. [Abstract] [Full Text] [PDF]
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 C. M. Ballantyne, R. C. Hoogeveen, H. Bang, J. Coresh, A. R. Folsom, L. E. Chambless, M. Myerson, K. K. Wu, A. R. Sharrett, and E. Boerwinkle Lipoprotein-Associated Phospholipase A2, High-Sensitivity C-Reactive Protein, and Risk for Incident Ischemic Stroke in Middle-aged Men and Women in the Atherosclerosis Risk in Communities (ARIC) Study Arch Intern Med, November 28, 2005; 165(21): 2479 - 2484. [Abstract] [Full Text] [PDF]
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J. M. Hill, M. A. Syed, A. E. Arai, T. M. Powell, J. D. Paul, G. Zalos, E. J. Read, H. M. Khuu, S. F. Leitman, M. Horne, et al. Outcomes and Risks of Granulocyte Colony-Stimulating Factor in Patients With Coronary Artery Disease J. Am. Coll. Cardiol., November 1, 2005; 46(9): 1643 - 1648. [Abstract] [Full Text] [PDF]
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S. H. Han, M. J. Quon, and K. K. Koh Beneficial Vascular and Metabolic Effects of Peroxisome Proliferator-Activated Receptor-{alpha} Activators Hypertension, November 1, 2005; 46(5): 1086 - 1092. [Abstract] [Full Text] [PDF]
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 A. M Carter Inflammation, thrombosis and acute coronary syndromes Diabetes and Vascular Disease Research, October 1, 2005; 2(3): 113 - 121. [Abstract] [PDF]
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H. Sun, T. Koike, T. Ichikawa, K. Hatakeyama, M. Shiomi, B. Zhang, S. Kitajima, M. Morimoto, T. Watanabe, Y. Asada, et al. C-Reactive Protein in Atherosclerotic Lesions: Its Origin and Pathophysiological Significance Am. J. Pathol., October 1, 2005; 167(4): 1139 - 1148. [Abstract] [Full Text] [PDF]
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P. Cirillo, P. Golino, P. Calabro, G. Cali, M. Ragni, S. De Rosa, G. Cimmino, M. Pacileo, R. De Palma, L. Forte, et al. C-reactive protein induces tissue factor expression and promotes smooth muscle and endothelial cell proliferation Cardiovasc Res, October 1, 2005; 68(1): 47 - 55. [Abstract] [Full Text] [PDF]
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T. Nakakuki, M. Ito, H. Iwasaki, Y. Kureishi, R. Okamoto, N. Moriki, M. Kongo, S. Kato, N. Yamada, N. Isaka, et al. Rho/Rho-Kinase Pathway Contributes to C-Reactive Protein-Induced Plasminogen Activator Inhibitor-1 Expression in Endothelial Cells Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2088 - 2093. [Abstract] [Full Text] [PDF]
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 T. Khreiss, L. Jozsef, L. A. Potempa, and J. G. Filep Loss of Pentameric Symmetry in C-Reactive Protein Induces Interleukin-8 Secretion Through Peroxynitrite Signaling in Human Neutrophils Circ. Res., September 30, 2005; 97(7): 690 - 697. [Abstract] [Full Text] [PDF]
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 M. Satoh, M. Nakamura, T. Akatsu, Y. Shimoda, I. Segawa, and K. Hiramori C-reactive protein co-expresses with tumor necrosis factor-{alpha} in the myocardium in human dilated cardiomyopathy Eur J Heart Fail, August 1, 2005; 7(5): 748 - 754. [Abstract] [Full Text] [PDF]
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A. Trion, M.P.M. de Maat, J.W. Jukema, A. van der Laarse, M.C. Maas, E.H. Offerman, L.M. Havekes, A.J. Szalai, H.M.G. Princen, and J.J. Emeis No Effect of C-Reactive Protein on Early Atherosclerosis Development in Apolipoprotein E*3-Leiden/Human C-Reactive Protein Transgenic Mice Arterioscler. Thromb. Vasc. Biol., August 1, 2005; 25(8): 1635 - 1640. [Abstract] [Full Text] [PDF]
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C. Liu, S. Wang, A. Deb, K. A. Nath, Z. S. Katusic, J. P. McConnell, and N. M. Caplice Proapoptotic, Antimigratory, Antiproliferative, and Antiangiogenic Effects of Commercial C-Reactive Protein on Various Human Endothelial Cell Types In Vitro: Implications of Contaminating Presence of Sodium Azide in Commercial Preparation Circ. Res., July 22, 2005; 97(2): 135 - 143. [Abstract] [Full Text] [PDF]
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I. Tarkun, B. Cetinarslan, E. Turemen, T. Sahin, Z. Canturk, and B. Komsuoglu Effect of rosiglitazone on insulin resistance, C-reactive protein and endothelial function in non-obese young women with polycystic ovary syndrome Eur. J. Endocrinol., July 1, 2005; 153(1): 115 - 121. [Abstract] [Full Text] [PDF]
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A. Pfutzner, N. Marx, G. Lubben, M. Langenfeld, D. Walcher, T. Konrad, and T. Forst Improvement of Cardiovascular Risk Markers by Pioglitazone Is Independent From Glycemic Control: Results From the Pioneer Study J. Am. Coll. Cardiol., June 21, 2005; 45(12): 1925 - 1931. [Abstract] [Full Text] [PDF]
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C. Arnaud, F. Burger, S. Steffens, N. R. Veillard, T. H. Nguyen, D. Trono, and F. Mach Statins Reduce Interleukin-6-Induced C-Reactive Protein in Human Hepatocytes: New Evidence for Direct Antiinflammatory Effects of Statins Arterioscler. Thromb. Vasc. Biol., June 1, 2005; 25(6): 1231 - 1236. [Abstract] [Full Text] [PDF]
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K. E. Taylor, J. C. Giddings, and C. W. van den Berg C-Reactive Protein-Induced In Vitro Endothelial Cell Activation Is an Artefact Caused by Azide and Lipopolysaccharide Arterioscler. Thromb. Vasc. Biol., June 1, 2005; 25(6): 1225 - 1230. [Abstract] [Full Text] [PDF]
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 B. Cariou, J.-C. Fruchart, and B. Staels Review: Vascular protective effects of peroxisome proliferator-activated receptor agonists The British Journal of Diabetes & Vascular Disease, May 1, 2005; 5(3): 126 - 132. [Abstract] [PDF]
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 The Diabetes Prevention Program Research Group Intensive Lifestyle Intervention or Metformin on Inflammation and Coagulation in Participants With Impaired Glucose Tolerance Diabetes, May 1, 2005; 54(5): 1566 - 1572. [Abstract] [Full Text] [PDF]
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Q. Wang, X. Zhu, Q. Xu, X. Ding, Y. E. Chen, and Q. Song Effect of C-reactive protein on gene expression in vascular endothelial cells Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1539 - H1545. [Abstract] [Full Text] [PDF]
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B. R. Clapp, G. M. Hirschfield, C. Storry, J. R. Gallimore, R. P. Stidwill, M. Singer, J. E. Deanfield, R. J. MacAllister, M. B. Pepys, P. Vallance, et al. Inflammation and Endothelial Function: Direct Vascular Effects of Human C-Reactive Protein on Nitric Oxide Bioavailability Circulation, March 29, 2005; 111(12): 1530 - 1536. [Abstract] [Full Text] [PDF]
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H.-K. Yip, C.-L. Hang, C.-Y. Fang, Y.-K. Hsieh, C.-H. Yang, W.-C. Hung, and C.-J. Wu Level of High-Sensitivity C-Reactive Protein Is Predictive of 30-Day Outcomes in Patients With Acute Myocardial Infarction Undergoing Primary Coronary Intervention Chest, March 1, 2005; 127(3): 803 - 808. [Abstract] [Full Text] [PDF]
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A. Chait, C. Y. Han, J. F. Oram, and J. W. Heinecke Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease? J. Lipid Res., March 1, 2005; 46(3): 389 - 403. [Abstract] [Full Text] [PDF]
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 A. G. Kaditis, E. I. Alexopoulos, E. Kalampouka, E. Kostadima, A. Germenis, E. Zintzaras, and K. Gourgoulianis Morning Levels of C-Reactive Protein in Children with Obstructive Sleep-disordered Breathing Am. J. Respir. Crit. Care Med., February 1, 2005; 171(3): 282 - 286. [Abstract] [Full Text] [PDF]
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Y. Ivashchenko, F. Kramer, S. Schafer, A. Bucher, K. Veit, V. Hombach, A. Busch, O. Ritzeler, J. Dedio, and J. Torzewski Protein Kinase C Pathway Is Involved in Transcriptional Regulation of C-Reactive Protein Synthesis in Human Hepatocytes Arterioscler. Thromb. Vasc. Biol., January 1, 2005; 25(1): 186 - 192. [Abstract] [Full Text] [PDF]
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D. E. Manolov, C. Rocker, V. Hombach, G. U. Nienhaus, and J. Torzewski Ultrasensitive Confocal Fluorescence Microscopy of C-Reactive Protein Interacting With Fc{gamma}RIIa Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2372 - 2377. [Abstract] [Full Text] [PDF]
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 I. Tarkun, B. C. Arslan, Z. Canturk, E. Turemen, T. Sahin, and C. Duman Endothelial Dysfunction in Young Women with Polycystic Ovary Syndrome: Relationship with Insulin Resistance and Low-Grade Chronic Inflammation J. Clin. Endocrinol. Metab., November 1, 2004; 89(11): 5592 - 5596. [Abstract] [Full Text] [PDF]
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H.-K. Yip, C.-J. Wu, H.-W. Chang, C.-H. Yang, K.-H. Yeh, S. Chua, and M. Fu Levels and Values of Serum High-Sensitivity C-Reactive Protein Within 6 Hours After the Onset of Acute Myocardial Infarction Chest, November 1, 2004; 126(5): 1417 - 1422. [Abstract] [Full Text] [PDF]
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 K. Kaushal, A. H. Heald, K. W. Siddals, M. S. Sandhu, D. B. Dunger, J. M. Gibson, and N. J. Wareham The Impact of Abnormalities in IGF and Inflammatory Systems on the Metabolic Syndrome Diabetes Care, November 1, 2004; 27(11): 2682 - 2688. [Abstract] [Full Text] [PDF]
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L. Li, N. Roumeliotis, T. Sawamura, and G. Renier C-Reactive Protein Enhances LOX-1 Expression in Human Aortic Endothelial Cells: Relevance of LOX-1 to C-Reactive Protein-Induced Endothelial Dysfunction Circ. Res., October 29, 2004; 95(9): 877 - 883. [Abstract] [Full Text] [PDF]
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T. Khreiss, L. Jozsef, L. A. Potempa, and J. G. Filep Opposing Effects of C-Reactive Protein Isoforms on Shear-Induced Neutrophil-Platelet Adhesion and Neutrophil Aggregation in Whole Blood Circulation, October 26, 2004; 110(17): 2713 - 2720. [Abstract] [Full Text] [PDF]
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P. J. Barter, S. Nicholls, K.-A. Rye, G.M. Anantharamaiah, M. Navab, and A. M. Fogelman Antiinflammatory Properties of HDL Circ. Res., October 15, 2004; 95(8): 764 - 772. [Abstract] [Full Text] [PDF]
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D. D. Sin, P. Lacy, E. York, and S. F. P. Man Effects of Fluticasone on Systemic Markers of Inflammation in Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., October 1, 2004; 170(7): 760 - 765. [Abstract] [Full Text] [PDF]
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 A. Recinos III, B. K. Carr, D. B. Bartos, I. Boldogh, J. R. Carmical, L. M. Belalcazar, and A. R. Brasier Liver gene expression associated with diet and lesion development in atherosclerosis-prone mice: induction of components of alternative complement pathway Physiol Genomics, September 16, 2004; 19(1): 131 - 142. [Abstract] [Full Text] [PDF]
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T.-S. Lee, C.-C. Chang, Y. Zhu, and J. Y.-J. Shyy Simvastatin Induces Heme Oxygenase-1: A Novel Mechanism of Vessel Protection Circulation, September 7, 2004; 110(10): 1296 - 1302. [Abstract] [Full Text] [PDF]
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 E. C. Suarez C-Reactive Protein Is Associated With Psychological Risk Factors of Cardiovascular Disease in Apparently Healthy Adults Psychosom Med, September 1, 2004; 66(5): 684 - 691. [Abstract] [Full Text] [PDF]
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D. Fliser, K. Buchholz, H. Haller, and for the EUropean Trial on Olmesartan and Pravastat Antiinflammatory Effects of Angiotensin II Subtype 1 Receptor Blockade in Hypertensive Patients With Microinflammation Circulation, August 31, 2004; 110(9): 1103 - 1107. [Abstract] [Full Text] [PDF]
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V. Pasceri, G. Patti, A. Nusca, C. Pristipino, G. Richichi, G. Di Sciascio, and on behalf of the ARMYDA Investigators Randomized Trial of Atorvastatin for Reduction of Myocardial Damage During Coronary Intervention: Results From the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) Study Circulation, August 10, 2004; 110(6): 674 - 678. [Abstract] [Full Text] [PDF]
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F. Blaschke, D. Bruemmer, F. Yin, Y. Takata, W. Wang, M. C. Fishbein, T. Okura, J. Higaki, K. Graf, E. Fleck, et al. C-Reactive Protein Induces Apoptosis in Human Coronary Vascular Smooth Muscle Cells Circulation, August 3, 2004; 110(5): 579 - 587. [Abstract] [Full Text] [PDF]
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K. E. Lewis, E. A. Kirk, T. O. McDonald, S. Wang, T. N. Wight, K. D. O'Brien, and A. Chait Increase in Serum Amyloid A Evoked by Dietary Cholesterol Is Associated With Increased Atherosclerosis in Mice Circulation, August 3, 2004; 110(5): 540 - 545. [Abstract] [Full Text] [PDF]
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K. K. Koh, M.-S. Shin, I. Sakuma, J. Y. Ahn, D. K. Jin, H. S. Kim, D. S. Kim, S. H. Han, W.-J. Chung, and E. K. Shin Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women Arterioscler. Thromb. Vasc. Biol., August 1, 2004; 24(8): 1516 - 1521. [Abstract] [Full Text] [PDF]
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 K. Prasad C-Reactive Protein Increases Oxygen Radical Generation by Neutrophils Journal of Cardiovascular Pharmacology and Therapeutics, July 1, 2004; 9(3): 203 - 209. [Abstract] [PDF]
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F Tomai C reactive protein and microvascular function Heart, July 1, 2004; 90(7): 727 - 728. [Abstract] [Full Text] [PDF]
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I. Jialal, S. Devaraj, and S. K. Venugopal C-Reactive Protein: Risk Marker or Mediator in Atherothrombosis? Hypertension, July 1, 2004; 44(1): 6 - 11. [Abstract] [Full Text] [PDF]
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 V. Pasceri and G. Cammarota C-Reactive Protein and Risk of Colon Cancer JAMA, June 16, 2004; 291(23): 2818 - 2819. [Full Text] [PDF]
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K. Amann, M.-L. Gross, and E. Ritz Pathophysiology Underlying Accelerated Atherogenesis in Renal Disease: Closing in on the Target J. Am. Soc. Nephrol., June 1, 2004; 15(6): 1664 - 1666. [Full Text] [PDF]
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 R. Tauman, A. Ivanenko, L. M. O'Brien, and D. Gozal Plasma C-Reactive Protein Levels Among Children With Sleep-Disordered Breathing Pediatrics, June 1, 2004; 113(6): e564 - e569. [Abstract] [Full Text]
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 R. Kleemann, L. Verschuren, B.-J. de Rooij, J. Lindeman, M. M. de Maat, A. J. Szalai, H. M. G. Princen, and T. Kooistra Evidence for anti-inflammatory activity of statins and PPAR{alpha} activators in human C-reactive protein transgenic mice in vivo and in cultured human hepatocytes in vitro Blood, June 1, 2004; 103(11): 4188 - 4194. [Abstract] [Full Text] [PDF]
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E. T.H. Yeh CRP as a Mediator of Disease Circulation, June 1, 2004; 109(21_suppl_1): II-11 - II-14. [Abstract] [Full Text] [PDF]
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C. Wadham, N. Albanese, J. Roberts, L. Wang, C. J. Bagley, J. R. Gamble, K.-A. Rye, P. J. Barter, M. A. Vadas, and P. Xia High-Density Lipoproteins Neutralize C-Reactive Protein Proinflammatory Activity Circulation, May 4, 2004; 109(17): 2116 - 2122. [Abstract] [Full Text] [PDF]
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 F. R. DANESH and Y. S. KANWAR Modulatory effects of HMG-CoA reductase inhibitors in diabetic microangiopathy FASEB J, May 1, 2004; 18(7): 805 - 815. [Abstract] [Full Text] [PDF]
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E. Paffen, H. L. Vos, and R. M. Bertina C-Reactive Protein Does Not Directly Induce Tissue Factor in Human Monocytes Arterioscler. Thromb. Vasc. Biol., May 1, 2004; 24(5): 975 - 981. [Abstract] [Full Text]
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S. Verma, P. E. Szmitko, and E. T.H. Yeh C-Reactive Protein: Structure Affects Function Circulation, April 27, 2004; 109(16): 1914 - 1917. [Full Text] [PDF]
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