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10.1152/ajprenal.00353.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00353.2014 C4166728!4166728 !25100282     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25100282 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Renal+Physiol 2014 ; 307 (6 ): F727-35 Nephropedia Template TP {{tp|p=25100282 |t=2014. Nitric oxide and carbon monoxide antagonize TGF-? through ligand-independent internalization of T?R1/ALK5 |pdf=|usr=}}{{25100282 }} gab.com Text Nitric oxide and carbon monoxide antagonize TGF- through ligand-independent internalization of T R1/ALK5 JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25100282 #FOAvip Transforming growth factor (TGF)-? plays a central role in vascular homeostasis and in the pathology of vascular disease. There is a growing appreciation for the role of nitric oxide (NO) and carbon monoxide (CO) as highly diffusible, bioactive signaling molecules in the vasculature. We hypothesized that both NO and CO increase endocytosis of TGF-? receptor type 1 (T?R1) in vascular smooth muscle cells (VSMCs) through activation of dynamin-2, shielding cells from the effects of circulating TGF-?. In this study, primary cultures of VSMCs from Sprague-Dawley rats were treated with NO-releasing molecule 3 (a NO chemical donor), CO-releasing molecule 2 (a CO chemical donor), or control. NO and CO stimulated dynamin-2 activation in VSMCs. NO and CO promoted time- and dose-dependent endocytosis of T?R1. By decreasing T?R1 surface expression through this dynamin-2-dependent process, NO and CO diminished the effects of TGF-? on VSMCs. These findings help explain an important mechanism by which NO and CO signal in the vasculature by decreasing surface expression of T?R1 and the cellular response to TGF-?. Twit Text FOAVip Nitric oxide and carbon monoxide antagonize TGF- through ligand-independent internalization of T R1/ALK5 ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25100282 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25100282 #FOAvip English Wikipedia <ref>{{Cite pmid|25100282 }}</ref> Nitric oxide and carbon monoxide antagonize TGF-? through ligand-independent internalization of T?R1/ALK5 #MMPMID25100282 Hovater MB ; Ying WZ ; Agarwal A ; Sanders PW Am J Physiol Renal Physiol 2014[Sep]; 307 (6 ): F727-35 PMID25100282 show ga Transforming growth factor (TGF)-? plays a central role in vascular homeostasis and in the pathology of vascular disease. There is a growing appreciation for the role of nitric oxide (NO) and carbon monoxide (CO) as highly diffusible, bioactive signaling molecules in the vasculature. We hypothesized that both NO and CO increase endocytosis of TGF-? receptor type 1 (T?R1) in vascular smooth muscle cells (VSMCs) through activation of dynamin-2, shielding cells from the effects of circulating TGF-?. In this study, primary cultures of VSMCs from Sprague-Dawley rats were treated with NO-releasing molecule 3 (a NO chemical donor), CO-releasing molecule 2 (a CO chemical donor), or control. NO and CO stimulated dynamin-2 activation in VSMCs. NO and CO promoted time- and dose-dependent endocytosis of T?R1. By decreasing T?R1 surface expression through this dynamin-2-dependent process, NO and CO diminished the effects of TGF-? on VSMCs. These findings help explain an important mechanism by which NO and CO signal in the vasculature by decreasing surface expression of T?R1 and the cellular response to TGF-?. |Animals [MESH] |Carbon Monoxide/*metabolism [MESH] |Dynamin II/metabolism [MESH] |Male [MESH] |Muscle, Smooth, Vascular/*metabolism [MESH] |Myocytes, Smooth Muscle/*metabolism [MESH] |Nerve Tissue Proteins/metabolism [MESH] |Nitric Oxide/*metabolism [MESH] |Polymerization [MESH] |Protein Serine-Threonine Kinases/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Receptor, Transforming Growth Factor-beta Type I [MESH] |Receptors, Transforming Growth Factor beta/metabolism [MESH] |T-Box Domain Proteins/metabolism [MESH]Nitric oxide and carbon monoxide antagonize TGF-? through ligand-indep(epmc).pdf DeepDyve Pubget Overpricing