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. Author manuscript; available in PMC: 2022 Jul 6.
Published in final edited form as: Circulation. 2021 Jun 3;144(1):52–73. doi: 10.1161/CIRCULATIONAHA.120.047978

Figure 1. Hypermethylation of BMPR2 promoter correlates with decreased SIN3a expression in human PAH and PAH-animal model.

Figure 1.

A. Methylation sites within the BMPR2 promoter region were identified by targeted-bisulfite sequencing. B. BMPR2 mRNA expression was analyzed by RT-qPCR in lung tissue from patients with idiopathic PAH (IPAH, n=5) and human non-PAH controls (n= 4). C. Upper panel, Representative BMPR2 and Cyclin D1 Western blot. Lower panel, the bar graph represents the quantification of BMPR2 and Cycin D1after correction for GAPDH by scanning densitometry. Data show fold stimulation with respect to control non-PAH. D. SIN3a mRNA expression was analyzed by RT-qPCR in lung homogenate tissue from patients with idiopathic PAH (IPAH, n=5) and non-PAH control lungs (n= 4). E. A representative blot of SIN3a protein expression (Upper Panel). Lower panel, bar graph represents the quantification of SIN3a correction for GAPDH. Data show fold stimulation with respect to control non-PAH. F. SIN3a mRNA expression was analyzed by RT-qPCR in lung tissue from control and MCT-induced PAH (n=3). G. SIN3a protein expression was assessed by Western blot in lung tissue from control and MCT-induced PAH (n=3). H. SIN3a mRNA expression was analyzed by RT-qPCR in lung tissue from control and Sugen Hypoxia-induced PAH mouse model (n=3). I. SIN3a protein expression was analyzed by western blot in lung tissue from control and Sugen Hypoxia-induced PAH mouse model (n=3). Data are presented as mean ±SEM; * = p<0.05, ** = p<0.01, *** P < 0.001.