Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI

被引:22
作者
Lee, Seul Gi [1 ]
Kim, Jin Soo [2 ]
Kim, Ha-Jeong [3 ]
Schlaepfer, David D. [4 ]
Kim, In-San [5 ,6 ]
Nam, Ju-Ock [1 ]
机构
[1] Kyungpook Natl Univ, Dept Food Sci & Biotechnol, Daegu 41566, South Korea
[2] Natl Inst Korean Med Dev, Kyeongsan 38540, South Korea
[3] Kyungpook Natl Univ, Sch Med, Dept Physiol, 680 Gukchaebosang Ro, Daegu 41944, South Korea
[4] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA
[5] Korea Univ, KU KIST Grad Sch Converging Sci & Technol, Seoul 02841, South Korea
[6] Korea Inst Sci & Technol KIST, Biomed Res Inst, Seoul 02792, South Korea
基金
新加坡国家研究基金会;
关键词
TISSUE ANGIOGENESIS; REGIONAL DIFFERENCES; GENE-EXPRESSION; CELL-ADHESION; OBESITY; GROWTH; BETA-IG-H3; FIBROSIS; MICE;
D O I
10.1038/s41598-021-88959-1
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页数:11
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