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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 Jun 6;33(8):1837–1843. doi: 10.1161/ATVBAHA.112.300752

Figure 4. PP2A inhibition abolished E2-mediated inhibition of kinase phosphorylation and VSMC proliferation.

Figure 4

(A) Western blot and quantification of PP2Ac, phosphorylated Akt and phosphorylated ERK. siRNA oligo targeting PP2Ac or non-targeting control was introduced into VSMC followed by E2 and PDGF treatment as described in Figure 2 (n=4). #P<0.05, *P<0.01. VSMC derived from WT mice was treated with vehicle (V) or E2 in the presence or absence of OA (50 nmol/L), and cell proliferation was assessed in each condition cultured with 3% sBGS (B) and PDGF (5 ng/ml) (C) (n=4 per each condition). #P<0.05 vs vehicle.