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Fig. 5 | Stem Cell Research & Therapy

Fig. 5

From: Let-7a-transfected mesenchymal stem cells ameliorate monocrotaline-induced pulmonary hypertension by suppressing pulmonary artery smooth muscle cell growth through STAT3-BMPR2 signaling

Fig. 5

The STAT3-BMPR2 signaling was responsible for MSC-let-7a-regulated growth inhibition of PASMCs. After co-culture with MSCs modified with let-7a or NC, the expression levels of STAT3, p-STAT3, and downstream BMPR2 were determined in PASMCs upon hypoxia by Western blotting. Cells cultured under normoxia were defined as the control group (a). Following treatment with the STAT3 inhibitor S31-201 (15 μM), the protein levels of BMPR2 in PASMCs were analyzed (b). Following preconditioning with BMPR2 siRNA for 24 h, the protein level of BMPR2 was determined by Western blotting (c). PASMCs were treated with BMPR2 siRNA and co-cultured with or without MSC-let-7a. Cell proliferation (d) and proliferation-related gene expression (including Ki67, cyclin D1, and PCNA) (e) were then determined. (f) Cell apoptosis was assessed by flow cytometry. *p < 0.05. BMPR2 bone morphogenetic protein receptor 2, MSC mesenchymal stem cell, NC miR-control, PCNA proliferating cell nuclear antigen, siRNA small interfering RNA, STAT3 signal transducers and activators of transcription 3

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