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10.1007/s11302-014-9442-3 http://scihub22266oqcxt.onion/10.1007/s11302-014-9442-3 C4336305!4336305!25563726     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Purinergic+Signal 2015 ; 11 (1): 139-53 Nephropedia Template TP {{tp|p=25563726|t=2015. Shear stress modulates endothelial KLF2 through activation of P2X4 |pdf=|usr=}}{{25563726}} gab.com Text Shear stress modulates endothelial KLF2 through activation of P2X4 JO: Purinergic Signal http://www.kidney.de/pget.php?&tw=1&pmid=25563726 #FOAvip Vascular endothelial cells that are in direct contact with blood flow are exposed to fluid shear stress and regulate vascular homeostasis. Studies report endothelial cells to release ATP in response to shear stress that in turn modulates cellular functions via P2 receptors with P2X4 mediating shear stress-induced calcium signaling and vasodilation. A recent study shows that a loss-of-function polymorphism in the human P2X4 resulting in a Tyr315>Cys variant is associated with increased pulse pressure and impaired endothelial vasodilation. Although the importance of shear stress-induced Krüppel-like factor 2 (KLF2) expression in atheroprotection is well studied, whether ATP regulates KLF2 remains unanswered and is the objective of this study. Using an in vitro model, we show that in human umbilical vein endothelial cells (HUVECs), apyrase decreased shear stress-induced KLF2, KLF4, and NOS3 expression but not that of NFE2L2. Exposure of HUVECs either to shear stress or ATP?S under static conditions increased KLF2 in a P2X4-dependent manner as was evident with both the receptor antagonist and siRNA knockdown. Furthermore, transient transfection of static cultures of human endothelial cells with the Tyr315>Cys mutant P2X4 construct blocked ATP-induced KLF2 expression. Also, P2X4 mediated the shear stress-induced phosphorylation of extracellular regulated kinase-5, a known regulator of KLF2. This study demonstrates a major physiological finding that the shear-induced effects on endothelial KLF2 axis are in part dependent on ATP release and P2X4, a previously unidentified mechanism.Electronic supplementary material: The online version of this article (doi:10.1007/s11302-014-9442-3) contains supplementary material, which is available to authorized users. Twit Text FOAVip Shear stress modulates endothelial KLF2 through activation of P2X4 ????Purinergic Signal http://www.kidney.de/pget.php?&tw=1&pmid=25563726 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25563726 #FOAvip English Wikipedia <ref>{{Cite pmid|25563726}}</ref> Shear stress modulates endothelial KLF2 through activation of P2X4 #MMPMID25563726 Sathanoori R; Rosi F; Gu BJ; Wiley JS; Müller CE; Olde B; Erlinge D Purinergic Signal 2015[Mar]; 11 (1): 139-53 PMID25563726show ga Vascular endothelial cells that are in direct contact with blood flow are exposed to fluid shear stress and regulate vascular homeostasis. Studies report endothelial cells to release ATP in response to shear stress that in turn modulates cellular functions via P2 receptors with P2X4 mediating shear stress-induced calcium signaling and vasodilation. A recent study shows that a loss-of-function polymorphism in the human P2X4 resulting in a Tyr315>Cys variant is associated with increased pulse pressure and impaired endothelial vasodilation. Although the importance of shear stress-induced Krüppel-like factor 2 (KLF2) expression in atheroprotection is well studied, whether ATP regulates KLF2 remains unanswered and is the objective of this study. Using an in vitro model, we show that in human umbilical vein endothelial cells (HUVECs), apyrase decreased shear stress-induced KLF2, KLF4, and NOS3 expression but not that of NFE2L2. Exposure of HUVECs either to shear stress or ATP?S under static conditions increased KLF2 in a P2X4-dependent manner as was evident with both the receptor antagonist and siRNA knockdown. Furthermore, transient transfection of static cultures of human endothelial cells with the Tyr315>Cys mutant P2X4 construct blocked ATP-induced KLF2 expression. Also, P2X4 mediated the shear stress-induced phosphorylation of extracellular regulated kinase-5, a known regulator of KLF2. This study demonstrates a major physiological finding that the shear-induced effects on endothelial KLF2 axis are in part dependent on ATP release and P2X4, a previously unidentified mechanism.Electronic supplementary material: The online version of this article (doi:10.1007/s11302-014-9442-3) contains supplementary material, which is available to authorized users. äShear stress modulates endothelial KLF2 through activation of P2X4 (epmc).pdf DeepDyve Pubget Overpricing