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首页> 外文期刊>Journal of cellular physiology. >HIFlA/miR-20a-5p/TGFpi axis modulates adipose-derived stem cells in a paracrine manner to affect the angiogenesis of human dermal microvascular endothelial cells
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HIFlA/miR-20a-5p/TGFpi axis modulates adipose-derived stem cells in a paracrine manner to affect the angiogenesis of human dermal microvascular endothelial cells

机译：HIFlA / miR-20a-5p TGFpi轴调节脂肪干细胞以旁分泌的方式影响人类皮肤的血管生成微血管内皮细胞

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摘要

Angiogenic cytokines secreted by the adipose-derived stem cells (ADSCs) might promote the angiogenesis of endothelial cells. In the present study, we hypothesize that miR-20a targets TGFB1 to modulate the transforming growth factor (31 (TGFβ1) secretion by ADSCs, therefore affecting the angiogenesis. We found that hypoxia-inducible factor 1A (HIF1A) and TGF(31 expressions were increased by hypoxia, accompanied with promoted ADSC cell viability. Incubation with conditioned medium from ADSCs treated with hypoxia significantly enhanced the angiogenesis capacity of human dermal microvascular endothelial cells (HDMECs), while TGFBl-silenced ADSCs medium significantly reverses HDMECs angiogenesis. miR-20a suppresses the expression of TGFB1 and secretion of TGF(31 by ADSCs via binding to its 3' untranslated region, therefore modulating the HDMEC angiogenesis via affecting the paracrine from ADSCs; the effects of miR-20a-overexpressed conditioned medium on HDMEC angiogenesis were significantly reversed by TGFBl-overexpressed conditioned medium. Finally, HIF1A suppressed the expression of miR-20a via targeting its promoter region, subsequently promoting the paracrine from ADSCs and HDMEC angiogenesis.
机译：血管生成细胞因子分泌的脂肪干细胞(ADSCs)可能促进内皮细胞的血管生成。本研究,我们假设miR-20aTGFB1调整转变经济增长目标因素(31 ADSCs (TGFβ1)分泌,因此影响血管生成。低氧诱导因子1 (HIF1A)和转化生长因子(31表达式是增加缺氧,伴随着提升ADSC细胞生存能力。孵化ADSCs条件培养基缺氧处理显著提高了人类皮肤的血管生成能力微血管内皮细胞(HDMECs)TGFBl-silenced ADSCs媒介显著逆转HDMECs血管再生。TGFB1的表达和分泌的TGF (31通过绑定ADSCs 3的翻译地区,因此调制HDMEC通过旁分泌的影响血管生成ADSCs;条件培养基上HDMEC血管生成显著逆转TGFBl-overexpressed条件培养基。针对其启动子的表达miR-20a通过地区,随后促进的旁分泌ADSCs HDMEC血管生成。

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