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10.1152/ajpcell.00275.2013 http://scihub22266oqcxt.onion/10.1152/ajpcell.00275.2013 C4329423!4329423!25472964     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Cell+Physiol 2015 ; 308 (4): C308-18 Nephropedia Template TP {{tp|p=25472964|t=2015. TRPM7 regulates vascular endothelial cell adhesion and tube formation |pdf=|usr=}}{{25472964}} gab.com Text TRPM7 regulates vascular endothelial cell adhesion and tube formation JO: Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25472964 #FOAvip Transient receptor potential melastatin 7 (TRPM7) is a nonselective cation channel with an ?-kinase domain in its COOH terminal, known to play a role in diverse physiological and pathological processes such as Mg2+ homeostasis, cell proliferation, and hypoxic neuronal injury. Increasing evidence suggests that TRPM7 contributes to the physiology/pathology of vascular systems. For example, we recently demonstrated that silencing TRPM7 promotes growth and proliferation and protects against hyperglycemia-induced injury in human umbilical vein endothelial cells (HUVECs). Here we investigated the potential effects of TRPM7 on morphology, adhesion, migration, and tube formation of vascular endothelial cells and the potential underlying mechanism. We showed that inhibition of TRPM7 function in HUVECs by silencing TRPM7 decreases the density of TRPM7-like current and cell surface area and inhibits cell adhesion to Matrigel. Silencing TRPM7 also promotes cell migration, wound healing, and tube formation. Further studies showed that the extracellular signal-regulated kinase (ERK) pathway is involved in the change of cell morphology and the increase in HUVEC migration induced by TRPM7 silencing. We also demonstrated that silencing TRPM7 enhances the phosphorylation of myosin light chain (MLC) in HUVECs, which might be involved in the enhancement of cell contractility and motility. Collectively, our data suggest that the TRPM7 channel negatively regulates the function of vascular endothelial cells. Further studies on the underlying mechanism may facilitate the development of the TRPM7 channel as a target for the therapeutic intervention of vascular diseases. Twit Text FOAVip TRPM7 regulates vascular endothelial cell adhesion and tube formation ????Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25472964 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25472964 #FOAvip English Wikipedia <ref>{{Cite pmid|25472964}}</ref> TRPM7 regulates vascular endothelial cell adhesion and tube formation #MMPMID25472964 Zeng Z; Inoue K; Sun H; Leng T; Feng X; Zhu L; Xiong ZG Am J Physiol Cell Physiol 2015[Feb]; 308 (4): C308-18 PMID25472964show ga Transient receptor potential melastatin 7 (TRPM7) is a nonselective cation channel with an ?-kinase domain in its COOH terminal, known to play a role in diverse physiological and pathological processes such as Mg2+ homeostasis, cell proliferation, and hypoxic neuronal injury. Increasing evidence suggests that TRPM7 contributes to the physiology/pathology of vascular systems. For example, we recently demonstrated that silencing TRPM7 promotes growth and proliferation and protects against hyperglycemia-induced injury in human umbilical vein endothelial cells (HUVECs). Here we investigated the potential effects of TRPM7 on morphology, adhesion, migration, and tube formation of vascular endothelial cells and the potential underlying mechanism. We showed that inhibition of TRPM7 function in HUVECs by silencing TRPM7 decreases the density of TRPM7-like current and cell surface area and inhibits cell adhesion to Matrigel. Silencing TRPM7 also promotes cell migration, wound healing, and tube formation. Further studies showed that the extracellular signal-regulated kinase (ERK) pathway is involved in the change of cell morphology and the increase in HUVEC migration induced by TRPM7 silencing. We also demonstrated that silencing TRPM7 enhances the phosphorylation of myosin light chain (MLC) in HUVECs, which might be involved in the enhancement of cell contractility and motility. Collectively, our data suggest that the TRPM7 channel negatively regulates the function of vascular endothelial cells. Further studies on the underlying mechanism may facilitate the development of the TRPM7 channel as a target for the therapeutic intervention of vascular diseases. äTRPM7 regulates vascular endothelial cell adhesion and tube formation (epmc).pdf DeepDyve Pubget Overpricing