Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

被引：4

作者：

Wang, Z. H. ^{[1
,2
]}

Zhu, W. ^{[1
]}

Tao, J. P. ^{[1
]}

Zhang, Q. Y. ^{[1
]}

Wei, M. ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 6, Div Cardiol, Shanghai 200223, Peoples R China

[2] Yancheng Peoples First Hosp, Div Cardiol, Yancheng, Jiangsu, Peoples R China

来源：

BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH | 2013年 / 46卷 / 11期

关键词：

Myocardial microvascular endothelial cells; Mast cell; Angiogenesis; Angiopoietin; Tie-2; GROWTH-FACTOR; IN-VIVO; ANGIOGENESIS; EXPRESSION; DENSITY; TRYPTASE; VEGF; INFLAMMATION; NETWORK; BARRIER;

D O I：

10.1590/1414-431X20132873

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Angiopoietin (Ang)-1 and Ang-2 interact in angiogenesis to activate the Tie-2 receptor, which may be involved in new vessel maturation and regression. Mast cells (MCs) are also involved in formation of new blood vessels and angiogenesis. The present study was designed to test whether MCs can mediate angiogenesis in myocardial microvascular endothelial cells (MMVECs). Using a rat MMVEC and MC co-culture system, we observed that Ang-1 protein levels were very low even though its mRNA levels were increased by MCs. Interestingly, MCs were able to enhance migration, proliferation, and capillary-like tube formation, which were associated with suppressed Ang-2 protein expression, but not Tie-2 expression levels. These MCs induced effects that could be reversed by either tryptase inhibitor [N-tosyl-L-lysine chloromethyl ketone (TLCK)] or chymase inhibitor (N-tosyl-L-phenylalanyl chloromethyl ketone), with TLCK showing greater effects. In conclusion, our data indicated that MCs can interrupt neovessel maturation via suppression of the Ang-2/Tie-2 signaling pathway.

引用

页码：920 / 928

页数：9

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