Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI.
Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI.
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DOI：
10.1038/s41598-021-88959-1
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发表时间：
2021-05-06
影响因子：
4.6
通讯作者：
Nam JO
中科院分区：
文献类型：
--
作者：
Lee SG;Kim JS;Kim HJ;Schlaepfer DD;Kim IS;Nam JO
一些研究表明，细胞外基质(ECM)重塑和微环境与脂肪生成和脂肪血管生成密切相关。在本研究中，我们证明了转化生长因子-β诱导(TGFBI)在体外和体内都能抑制脂肪细胞条件培养液(Ad-CM)刺激的血管生成。TGFBI基因敲除(KO)小鼠脂肪组织中的血管数量增加，这些小鼠的血管对含有Ad-CM的Matrigel的渗透增强。用TGFBI蛋白处理Ad-CM刺激的Svec-10内皮细胞后，细胞的迁移和成管活性降低。TGFBI蛋白抑制这些Svec-10内皮细胞的Src和细胞外信号相关激酶信号通路的激活。我们的结果表明，TGFBI通过抑制Src和ERK信号通路的激活而抑制脂肪血管生成，可能与刺激内皮细胞的血管生成活性有关。
Several studies have suggested that extracellular matrix (ECM) remodeling and the microenvironment are tightly associated with adipogenesis and adipose angiogenesis. In the present study, we demonstrated that transforming growth factor-beta induced (TGFBI) suppresses angiogenesis stimulated by adipocyte-conditioned medium (Ad-CM), both in vitro and in vivo. TGFBI knockout (KO) mice exhibited increased numbers of blood vessels in adipose tissue, and blood vessels from these mice showed enhanced infiltration into Matrigel containing Ad-CM. The treatment of Ad-CM-stimulated SVEC-10 endothelial cells with TGFBI protein reduced migration and tube-forming activity. TGFBI protein suppressed the activation of the Src and extracellular signaling-related kinase signaling pathways of these SVEC-10 endothelial cells. Our findings indicated that TGFBI inhibited adipose angiogenesis by suppressing the activation of Src and ERK signaling pathways, possibly because of the stimulation of the angiogenic activity of endothelial cells.
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