| 卵泡抑素样蛋白1促进肺动脉内皮细胞增生、黏附与血管生成 |
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| 引用本文： | 沙宇惠,高阳,刘杰,齐先梅,韩璐璐,王望. 卵泡抑素样蛋白1促进肺动脉内皮细胞增生、黏附与血管生成[J]. 首都医科大学学报, 2020, 41(1): 80-86. DOI: 10.3969/j.issn.1006-7795.2020.01.016 |
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| 作者姓名： | 沙宇惠 高阳 刘杰 齐先梅 韩璐璐 王望 |
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| 作者单位： | 首都医科大学基础医学院,北京100069;首都医科大学基础医学院,北京100069;首都医科大学基础医学院生理学与病理生理学系,北京100069 |
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| 基金项目： | 国家自然科学基金（31600939），北京市自然科学基金（7174280），北京市优秀人才培养资助项目（2015000020124G111），首都医科大学科研创新基金资助项目（XSKY2018014）。 |
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| 摘 要： | 目的 探究卵泡抑素样蛋白1（follistatin-like 1，FSTL1）对人肺动脉内皮细胞（human pulmonary artery endothelial cells，HPAECs）的影响，完善FSTL1在肺动脉高压（pulmonary hypertension，PH）中的作用。方法 以人肺动脉内皮细胞为对象，使用qRT-PCR和Western blotting法测定低氧刺激下HPAECs中FSTL1的表达水平。通过给予外源性FSTL1蛋白或小干扰RNA，MTT法观察FSTL1对细胞增生活性的影响。分别借助纤连蛋白、Matrigel基质胶观察FSTL1对内皮细胞黏附与血管形成能力的影响。结果 低氧刺激HPAECs 12 h和24 h后，FSTL1的mRNA及蛋白质的表达量均提高（P<0.01）。常氧下外源给予FSTL1，250 μg/L、500 μg/L组的细胞增生活性与对照组相比明显增高（P<0.01）；低氧条件下siRNA干扰组HPAECs增生活性与对照组相比明显降低（P<0.001）。常氧下外源给予250 μg/L的FSTL1刺激24 h后HPAECs黏附数量增多（P<0.001），生成血管总长度及新生血管数目均增加（P<0.001）。结论 FSTL1促进HPAECs增生、黏附与血管生成。
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| 关 键 词： | 肺动脉高压 低氧 卵泡抑素样蛋白1(FSTL1) 人肺动脉内皮细胞 |
| 收稿时间： | 2019-07-12 |
FSTL1 promotes proliferation,adhesion and tube formation of pulmonary artery endothelial cells |
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| 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. DOI: 10.3969/j.issn.1006-7795.2020.01.016 |
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| Authors: | Sha Yuhui Gao Yang Liu Jie Qi Xianmei Han Lulu Wang Wang |
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| Affiliation: | 1. School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China;2. Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China |
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| 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. |
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| Keywords: | pulmonary hypertension hypoxia follistatin-like 1(FSTL1) human pulmonary artery endothelial cells |
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