FSTL1 promotes proliferation, adhesion and tube formation of pulmonary artery endothelial cells

doi:10.3969/j.issn.1006-7795.2020.01.016

Abstract

Abstract: Objective To investigate the effect of follistatin-like 1(FSTL1) on human pulmonary artery endothelial cells (HPAECs) and to replenish the role of FSTL1 in pulmonary hypertension (PH). Methods The levels of FSTL1 in HPAECs were evaluated by qRT-PCR and Western blotting. Cellular viability was determined by MTT after giving exogenous recombinant human FSTL1 or small interfering RNA (siRNA). We also observed the effect of FSTL1 on adhesion and angiogenesis in HPAECs. Results Exposure to hypoxia upregulated the expression of FSTL1 mRNA and protein in HPAECs (P<0.01). The cellular viability of HPAECs stimulated by FSTL1 250 μg/L and 500 μg/L were higher than FSTL1 0 μg/L group under normoxia (P<0.01). SiRNA-mediated knockdown of FSTL1 attenuated hypoxia-induced proliferation of HPAECs compared with the negative control group (P<0.001). The amount of adherent cells stimulated with FSTL1 250 μg/L was increased under normoxia compared with that in the control group (P<0.001). The total length and the amount of tubes formed by HPAECs stimulated with FSTL1 250 μg/L were both increased under normoxia compared with the control group (P<0.001). Conclusions FSTL1 promotes proliferation, adhesion and tube formation of HPAECs.

Key words: pulmonary hypertension, hypoxia, follistatin-like 1(FSTL1), human pulmonary artery endothelial cells

CLC Number:

R363.2

Sha Yuhui, Gao Yang, Liu Jie, Qi Xianmei, Han Lulu, Wang Wang. FSTL1 promotes proliferation, adhesion and tube formation of pulmonary artery endothelial cells[J]. Journal of Capital Medical University, 2020, 41(1): 80-86.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2020.01.016

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2020/V41/I1/80

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