Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free free
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Myosin light chain kinase in microvascular endothelial barrier function Shen Q; Rigor RR; Pivetti CD; Wu MH; Yuan SYCardiovasc Res 2010[Jul]; 87 (2): 272-80Microvascular barrier dysfunction is implicated in the initiation and progression of inflammation, posttraumatic complications, sepsis, ischaemia-reperfusion injury, atherosclerosis, and diabetes. Under physiological conditions, a precise equilibrium between endothelial cell-cell adhesion and actin-myosin-based centripetal tension tightly controls the semi-permeability of microvascular barriers. Myosin light chain kinase (MLCK) plays an important role in maintaining the equilibrium by phosphorylating myosin light chain (MLC), thereby inducing actomyosin contractility and weakening endothelial cell-cell adhesion. MLCK is activated by numerous physiological factors and inflammatory or angiogenic mediators, causing vascular hyperpermeability. In this review, we discuss experimental evidence supporting the crucial role of MLCK in the hyperpermeability response to key cell signalling events during inflammation. At the cellular level, in vitro studies of cultured endothelial monolayers treated with MLCK inhibitors or transfected with specific inhibiting peptides have demonstrated that induction of endothelial MLCK activity is necessary for hyperpermeability. Ex vivo studies of live microvessels, enabled by development of the isolated, perfused venule method, support the importance of MLCK in endothelial permeability regulation in an environment that more closely resembles in vivo tissues. Finally, the role of MLCK in vascular hyperpermeability has been confirmed with in vivo studies of animal disease models and the use of transgenic MLCK210 knockout mice. These approaches provide a more complete view of the role of MLCK in vascular barrier dysfunction.|*Capillary Permeability/drug effects/genetics[MESH]|Actomyosin/metabolism[MESH]|Animals[MESH]|Body Fluids/*metabolism[MESH]|Cells, Cultured[MESH]|Endothelium, Vascular/drug effects/*enzymology/immunology/physiopathology[MESH]|Humans[MESH]|Inflammation Mediators/metabolism[MESH]|Inflammation/enzymology/physiopathology[MESH]|Mice[MESH]|Mice, Transgenic[MESH]|Microvessels/drug effects/*enzymology/immunology/physiopathology[MESH]|Models, Animal[MESH]|Myosin Light Chains/metabolism[MESH]|Myosin-Light-Chain Kinase/antagonists & inhibitors/genetics/*metabolism[MESH]|Phosphorylation[MESH]|Protein Kinase Inhibitors/pharmacology[MESH]|Signal Transduction[MESH] |