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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2016 Aug;68(2):127–142. doi: 10.1097/FJC.0000000000000395

Figure 4. mPGES-1 inhibition increases hASMC differentiation.

Figure 4

Following treatment with the mPGES-1 inhibitor 15d-PGJ2 or the COX-2 inhibitor celecoxib (Cel, 2 µM) for 1 day in de-differentiation conditions, hASMCs were analyzed for (A) PGE2 in the culture media, or (B) α-actin protein expression by immunohistochemistry. (C) hASMCs were also treated with 15d-PGJ2 in serum-free conditions and analyzed for α-actin protein expression by immunohistochemistry. (D) hASMCs were treated with rosiglitazone under de-differentiation (d-DC) and serum-free conditions (SFC) and analyzed for α-actin protein expression by immunohistochemistry. (E) hASMCs were treated for 1 day with 15d-PGJ2 or celecoxib (Cel, 2 µM) under de-differentiation conditions and analyzed for the stable PGI2 product 6-keto PG F1α in the culture media. (F) hASMCs were treated with 15d-PGJ2 or celecoxib (Cel, 2 µM) under de-differentiation conditions and analyzed for the stable TXA2 product TXB2. The data represent mean + SEM (n=4), * = p < 0.05, *** = p < 0.001, and **** = p < 0.0001; one-way ANOVA.