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. Author manuscript; available in PMC: 2011 Jul 23.
Published in final edited form as: Circ Res. 2010 May 20;107(2):271–282. doi: 10.1161/CIRCRESAHA.110.219899

Figure 2. PTH and the constitutively active receptor caPTH1R inhibit canonical Wnt/β-catenin signaling, Col1A1 transcription, and collagen accumulation.

Figure 2

Figure 2

Figure 2

Figure 2

Figure 2

Figure 2

Panel A, A7r5 aortic VSMCs were transfected with the TOPLUC reporter and treated with 10 ng/ml Wnt3a and 100 nM PTH either alone or in combination. PTH(1–34) abrogated Wnt3a-mediated activation (n = 6 per condition, replicated twice). Panel B, PTH(1–34) inhibits SFG-Wnt7a and SFG-Wnt7b induction of Col1A1 and Col1A2 expression in transduced primary aortic VSMCs (n = 3 per condition, replicated twice). Panel C, co-transfection of SM-caPTH1R, a VSMC expression plasmid for constitutively active caPTH1R, also inhibits TOPLUC activation by pcDNA3-Wnt7a or pcDNA-Wnt7b (n = 6 per condition, replicated twice). Panel D, TOPLUC inhibition by SM-caPTH1R was promoter-specific, since SM-caPTH1R stimulates pCRE-LUC (n = 6 per condition, replicated twice). Panel E, SM-caPTH1R inhibits basal and pcDNA3-Wnt7a induced Col1A1 promoter activity (n = 6 per condition, replicated 4 times). Panel F, primary aortic VSMC transduced with SFG-caPTH1R exhibit decreased collagen protein accumulation vs. SFG-LacZ controls (n = 3 per condition).