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. Author manuscript; available in PMC: 2013 Aug 2.
Published in final edited form as: J Am Coll Cardiol. 2011 Jun 21;57(25):2527–2538. doi: 10.1016/j.jacc.2011.02.037

Figure 5. Regulation of Cell Cycle–Controlling Proteins Through PI3K and PLCγ.

Figure 5

(A) Platelet-derived growth factor (PDGF)-BB causes induction of cyclin D1 and down-regulation of p27 kip1 protein at 24 h, resulting in retinoblastoma protein phosphorylation (P-Rb). (B) The activated chimeric receptor wild type (ChiR-WT) mimics the PDGF-BB–induced response in naive vascular smooth muscle cells (VSMCs). (C) Regulation of cyclin D1 and p27 kip1 by the ligand-induced F40/51 and F1021 mutants. (D) Regulation of cyclin D1 and p27 kip1 by the ligand-induced Y40/51 and Y1021 mutants. (E) Naive VSMCs were treated with 50 ng/ml of PDGF-BB for 24 h in the presence of pharmacological inhibitors of phosphatidylinositol 3-kinase (PI3K; LY294002) or phospholipase Cγ 1 (PLCγ; U73122). (B to D) Cyclin D1 and p27kip1 signals were scanned and quantified by densitometry, and the values were normalized for GTPase activating protein of ras (RasGAP) levels (lysate control). Data represent mean ± standard error of the mean from 3 independent experiments (*p < 0.05, #p < 0.01 vs. buffer).