Clin Res Cardiol 100, Suppl 1, April 2011

P653 - Ciglitazone Selectively Inhibits Vascular Smooth Muscle Cell Proliferation in Murine Embryonic Stem Cells
T. Pörner1, C. Danzer1, S. Otto1, H.-R. Figulla1, M. Wartenberg1
1Klinik für Innere Medizin I, Universitätsklinikum Jena, Jena;
Background: Peroxisome proliferator-activated receptor-gamma (PPARg) agonists improve insulin resistance and exert anti-inflammatory, anti-oxidative and anti-proliferative effects on vascular wall cells. Aim of the study was to assess the action of different PPARg agonists on endothelial- (EC) and vascular smooth muscle cell (VSMC) differentiation and proliferation in murine embryonic stem cells.
Methods: Embryoid bodies from CGR8 mouse stem cells were plated on day 4 and incubated with rosiglitazone 10 µM and ciglitazone 10µM either alone or in co-incubation with the PPARg antagonist GW9662 (10 µM). Differentiation of EC was assessed on days 12, 14, 16 and 18 by confocal laser scanning microscopy with CD31 staining. VSMC was stained with alpha smooth muscle act in (aSMC) and quantified by western blot on days 12 and 18.
Results: As shown in Fig. 1, rosiglitazone induced a stronger inhibition of EC differentiation at all time points as compared to ciglitazone. On the contrary, proliferation of VSMC at western blot was significantly stronger inhibited after incubation with ciglitazone alone (Fig. 2). This finding was not fully reversed under co-incubation with the PPARg antagonist GW9662.
Conclusions: PPARg agonist ciglitazone selectively suppresses VSMC growth with less inhibition of EC differentiation compared to rosiglitazone, possibly due to specific pleiotropic effects beyond PPARg activation. Thus, ciglitazone might be useful as a local therapy to inhibit restenosis after stent implantation.



Clin Res Cardiol 100, Suppl 1, April 2011
Zitierung mit Vortrags- oder Posternummer s.o.
DOI 10.1007/s00392-011-1100-y