Angiotensin Type 1 Receptor Blockers Induce Peroxisome ProliferatorActivated Receptor-
Activity
Circulation Schupp et al.
109: 2054
Data Supplement
Files in this Data Supplement:
- Figure
-
(TIFF) (1.83 MB). A, The PPARγ antagonist GW9662 inhibits ARB-induced aP2 expression. 3T3-L1 cells were differentiated with Mix (without IBMX) plus pioglitazone (1 μmol/L), telmisartan (10 μmol/L), or irbesartan (100 μmol/L) in the absence and presence of the PPARγ antagonist GW9662 (GW) (30 μmol/L). After 6 days, aP2 mRNA was quantified with the use of real-time PCR. Expression of aP2 was normalized to 18S expression. Experiments were repeated 3 times; results are shown as percentage of cells stimulated with pioglitazone/ARBs without GW. Data are presented as mean±SD. *P<0.05, #P<0.01 vs GW-untreated cells. B, ARBs induce PPARγ activity. 3T3-L1 cells were transfected with PPRE-luciferase reporter construct before stimulation with pioglitazone (10 μmol/L), eprosartan (10+100 μmol/L), losartan (10+100 μmol/L), irbesartan (10 μmol/L), and telmisartan (10 μmol/L). Firefly luciferase activity was measured after 24 hours and normalized with activity of cotransfected renilla luciferase. Experiments were repeated 3 times; results are presented as mean±SD. *P<0.05, #P<0.01 vs vehicle-treated cells.