Premium
Endothelial MLCK Contributes to Microvascular Leakage in Thermal Trauma
Author(s) -
Reynoso Rashell,
Breslin Jerry W.,
Watterson D. Martin,
Watson Katherine D.,
Wu Mack H.,
Yuan Sarah Y.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb15-a
Subject(s) - leakage (economics) , medicine , chemistry , cardiology , economics , macroeconomics
Microvascular leakage has been implicated in the pathogenesis of multiple organ injuries during trauma. Previous studies suggest the involvement of myosin light chain (MLC) phosphorylation‐triggered endothelial contraction in the development of microvascular hyperpermeability. The goal of this study was to further investigate the mechanism of MLC‐dependent barrier injury, focusing on endothelial‐specific MLC kinase (eMLCK). A genetic mouse model of eMLCK−/− was subjected to 3 rd degree burn covering 25% total body surface. The mesentery was observed using intravital microscopy, and microvascular permeability was assessed by measuring transvenular flux of FITC‐albumin (initial i.v. bolus 15 mg/kg followed by 0.15 mg/kg/min). The fluorescence intensities were collected from inside (Ii) and outside (Io) a selected venule, and the tracer flux was determined by the ratio of its transmural intensity difference to its intraluminal intensity normalized to the background, calculated as 1‐(Ii‐Io)/Ii. The results show that microvascular leakage after burn is significantly attenuated in eMLCK−/− mice compared to WT. We suggest that eMLCK is involved in burn‐induced microvascular hyperpermeability. Supported by HL70752, 61507, 73324, and 76079.