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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Atherosclerosis. 2012 Dec 19;227(1):65–71. doi: 10.1016/j.atherosclerosis.2012.12.003

Fig. 1.

Fig. 1

Anti-mitogenic effect of ApoE3 linked to p27 and the Cox2-PGI2-IP pathway in VSMCs. (A) Serum-starved early passage VSMCs from wild type and IP-null mice were stimulated with 10% FBS in the absence (control; C) or presence of cicaprost (Cica), apoE3, apoE3 with nimesulide (nim; Cox-2 inhibitor), or apoE3 with SC560 (SC; Cox-1 inhibitor). VSMCs were collected after 24 h, lysed, and immunoblotted for p27 and actin (loading control). The vertical white bar in the blot of IP-null VSMCs indicates where extraneous lanes were removed. Results from 3 to 6 independent experiments were quantified using Image J and combined to show mean ± SD. (B) VSMCs were prepared as in A but treated with cicaprost and apoE3, alone and in combination. Lysates were analyzed by immunoblotting for p27 and GAPDH (loading control). Results from 3 independent experiments were quantified using Image J and combined to show mean ± SD. (C) Serum-starved VSMCs from wild-type and p27-null mice were stimulated with 10% FBS in the absence or presence of cicaprost or apoE3 for 48 h; coverslips were analyzed for BrdU incorporation by immunofluorescence microscopy. Results are plotted as mean ± SD, n = 4. For all panels, *p < 0.05. **p < 0.01. ***p < 0.001 as determined by 2-tailed t-test.