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PPAR γ  ligands have been shown to have antiproliferative effects on many cell types. We herein report that a synthetic dominant-negative (DN) PPAR γ  mutant functions like a growth factor to promote cell cycle progression and cell proliferation in human coronary artery smooth muscle cells (CASMCs). In quiescent CASMCs, adenovirus-expressed DN-PPAR γ  promoted G1→S cell cycle progression, enhanced BrdU incorporation, and increased cell proliferation. DN-PPAR γ  expression also markedly enhanced positive regulators of the cell cycle, increasing Rb and CDC2 phosphorylation and the expression of cyclin A, B1, D1, and MCM7. Conversely, overexpression of wild-type (WT) or constitutively-active (CA) PPAR γ  inhibited cell cycle progression and the activity and expression of positive regulators of the cell cycle. DN-PPAR γ  expression, however, did not up-regulate positive cell cycle regulators in PPAR γ -deficient cells, strongly suggesting that DN-PPAR γ  effects on cell cycle result from blocking the function of endogenous wild-type PPAR γ . DN-PPAR γ  expression enhanced phosphorylation of ERK MAPKs. Furthermore, the ERK specific-inhibitor PD98059 blocked DN-PPAR γ -induced phosphorylation of Rb and expression of cyclin A and MCM7. Our data thus suggest that DN-PPAR γ  promotes cell cycle progression and cell growth in CASMCs by modulating fundamental cell cycle regulatory proteins and MAPK mitogenic signaling pathways in vascular smooth muscle cells (VSMCs).

ppar research

A Dominant-Negative PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>Mutant Promotes Cell Cycle Progression and Cell Growth in Vascular Smooth Muscle Cells

A Dominant-Negative PPARγMutant Promotes Cell Cycle Progression and Cell Growth in Vascular Smooth Muscle Cells