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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Biochem Pharmacol. 2018 Mar 30;152:187–200. doi: 10.1016/j.bcp.2018.03.027

Fig. 6.

Fig. 6

AngII-induced ERK1/2 phosphorylation in primary VSMCs and effects of CaM antagonism. (A & B) Bright-field images of primary porcine endothelial cells (PAECs, A) and VSMCs (B) isolated from the same porcine aortas cultured in phenol red-containing medium for visualization purposes. Images were taken using a Moticam CMOS camera (Motic Microscopes). (C) Immunoblots for smooth muscle α-actin (lower) and β-actin (upper) from lysates of the PAECs and VSMCs isolated. (D) Primary VSMCs were serum starved for 4 hrs prior to pretreatment with or without losartan (1 μM) or W-7 (100 μM) for 30 minutes, followed by treatment for 10 minutes with vehicle or 100 nM AngII. Upper immunoblot, representative changes in phosphorylated ERK1/2; lower immunoblot, corresponding total ERK1/2 expression, reprobed from stripped upper membrane. Histogram, average (n = 6 independent experiments) relative AT1R-mediated ERK1/2 phosphorylation in response to specified treatment. Densitometric values of the phosphorylated ERK1/2 bands were divided by corresponding values for total ERK1/2 bands and normalized.