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Local thermal injury induces general endothelial cell contraction through p38 MAP kinase activation
Author(s) -
Wang Shuyun,
Huang Qiaobing,
Guo Jingxin,
Guo Xiaohua,
Sun Quanmei,
Brunk Ulf T.,
Han Dong,
Zhao Kesen,
Zhao Ming
Publication year - 2014
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12226
Subject(s) - stress fiber , contraction (grammar) , microbiology and biotechnology , tight junction , actin , p38 mitogen activated protein kinases , inflammation , chemistry , confocal microscopy , kinase , protein kinase a , endothelial stem cell , biophysics , biology , phosphorylation , immunology , biochemistry , focal adhesion , endocrinology , in vitro
Endothelial cells ( EC s) of thin‐walled blood vessels form a barrier between blood and tissue. As a response to inflammation, the EC junctions widen and gaps form, resulting in compromised barrier functions. Although the mechanisms behind the establishment of these changes are still incompletely understood, one known reason is actomyosin‐dependent actin rearrangement. Here, by using atomic force microscopy and a combination of confocal microscopy methods, we are the first to report that thermal injury induces general venular hyperpermeability and that serum from burned rats induces EC actin rearrangement, contraction, as well as tight‐junction damage. Inhibition of the p38 mitogen‐activated protein kinase (p38MAPK) largely ameliorates resulting vascular dysfunction by significantly reducing EC stress‐fiber formation, contraction, volume changes and tight‐junction damage, thereby greatly reducing the appearance of EC gaps. The findings may be of importance for the design of future pharmacotherapies aiming to ease the severe general vascular dysfunction that follows extensive burns.