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Ischemia/reperfusion and cytokines: effects on coronary endothelial cytoskeleton and permeability
Author(s) -
Tinsley John H
Publication year - 2007
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.21.5.a488-a
Subject(s) - extravasation , cytokine , evans blue , medicine , endothelium , ischemia , endothelial stem cell , cytoskeleton , reperfusion injury , myosin light chain kinase , vascular permeability , microbiology and biotechnology , proinflammatory cytokine , inflammation , chemistry , actin , pathology , biology , cell , in vitro , biochemistry
Conditions such as myocardial infarction and ischemia/reperfusion (I/R) injury to the heart lead to the release of cytokines such as IL‐1β IL‐6, and TNFα. Subsequent to cytokine release, changes occur with regard to structure and function of the coronary microvascular endothelium. Specifically, signaling pathways become activated and cytoskeletal alterations become apparent. However, the exact molecular mechanisms controlling these cytokine‐induced modifications are poorly understood. The objective of these studies is to determine the specific cellular events that lead to cytokine‐induced endothelial dysfunction, a malady that leads to coronary tissue damage. Treatment of a rat heart microvascular endothelial cell line with the above‐mentioned cytokines led to an increase in permeability as measured by FITC‐albumin flux across the monolayer. In addition, the cytokines induced myosin light chain phosphorylation and actin stress fiber formation. Progression of this work to an in vivo model showed that cytokines administered by IV to the rat induced increases in extravasation of Evans blue from the circulation to heart tissue. Also, I/R injury, induced by clamping and subsequent release of the left coronary artery, resulted in increases in both TNFα release and protein extravasation. This work supported by Scott and White Memorial Hospital Dept. of Surgery.