Local thermal injury induces general endothelial cell contraction through p38 MAP kinase activation
2014 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, no 9, 832-841 p.Article in journal (Refereed) Published
Endothelial cells (ECs) 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.
Place, publisher, year, edition, pages
Wiley , 2014. Vol. 122, no 9, 832-841 p.
endothelial cells; thermal injury; contraction; permeability; p38 MAPK
IdentifiersURN: urn:nbn:se:liu:diva-110963DOI: 10.1111/apm.12226ISI: 000341151300016PubMedID: 24479891OAI: oai:DiVA.org:liu-110963DiVA: diva2:752271
Funding Agencies|National Natural Science Foundation of China [81071549, 81272095]; Natural Science Foundation of Guangdong province [2012B050600002]; Guangdong province talent recruitment foundation; Guangdong Innovative Research Team Program [201001Y0104675344]; Guangdong province university Qianbaishi program2014-10-032014-10-012014-10-03