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. 2019 Nov 18;51(11):137. doi: 10.1038/s12276-019-0330-3

Fig. 3. DP1- and DP2-independent VSMC phenotypic changes induced by PGD2.

Fig. 3

a P4-stage VSMCs were stimulated with the indicated prostanoids or a thromboxane analog (U46619) for 4 days. Cell lysates were examined for the expression of SMA and SM22α. b P4-stage VSMCs were stimulated with TNFα or PGD2 for 4 days, and AngII-dependent contraction was analyzed (n = 2). *P < 0.05 compared with the no-treatment (NT) group. c P4-stage VSMCs were pretreated with the indicated inhibitors (PD, PD98059; SP, SP600125; SB, SB203580), and PGD2-dependent changes in the expression of SMA and SM22α were assessed. d P4-stage VSMCs were pretreated with a MEK, DP1, or DP2 inhibitor (PD98059, BWA868C, or TM-30089) and then stimulated with PGD2. Cell lysates were analyzed for ERK activation. e P4-stage VSMCs were stimulated with a DP1 or DP2 agonist (BW245C (upper panel) or DK-PGD2 (lower panel)), and ERK activation was assessed. f P4-stage VSMCs were pretreated with a DP1 or DP2 antagonist (BWA868C or TM-30089), and PGD2-dependent gene expression changes in SMA and SM22α were examined. g P4-stage VSMCs were stimulated with a DP1 or DP2 agonist (BW245C (upper panel) or DK-PGD2 (lower panel)), and the expression levels of SMA and SM22α were assessed. The results are presented as the means ± SEM. One-way ANOVA and Tukey’s multiple comparison test were used to determine the P values. The asterisks indicate statistical significance (P < 0.05).