PTPRM - Endothelial Cell Adhesion

Endothelial Cell Adhesion

PTPµ is expressed in human umbilical cord vein endothelial cells (HUVEC) and in capillaries in the developing brain. The expression of PTPµ in HUVEC cells increases at higher cell density. Studies of PTPµ expression in animal tissues have demonstrated that PTPµ is preferentially expressed in endothelial cells of arteries and capillaries and in cardiac smooth muscle, in addition to brain cells. Because of this specialized expression in arterial endothelial cells, and because PTPµ is found to associate with proteins involved in maintaining endothelial cell–cell junctions, such as VE-cadherin, PTPµ is hypothesized to regulate endothelial cell junction formation or permeability. PTPµ has been shown to be involved in mechanotransduction that results from changes in blood flow to influence endothelial cell-mediated blood vessel dilation, a process induced by “shear stress.” When PTPmu is missing in mice (PTPmu -/- knock-out mice), cannulated mesenteric arteries show reduced flow-induced (or “shear stress” induced) dilation. PTPmu tyrosine phosphatase activity is activated by shear stress. Caveolin 1 is a scaffolding protein enriched in endothelial cell junctions that is also linked to shear stress regulated responses. Caveolin 1 is dephosphorylated on tyrosine 14 in response to shear stress and PTPmu is hypothesized to catalyze this reaction.

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