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10.1038/ki.2013.219 http://scihub22266oqcxt.onion/10.1038/ki.2013.219 23760283!ä!23760283 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23760283.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Kidney+Int 2013 ; 84 (6): 1198-206 Nephropedia Template TP {{tp|p=23760283|t=2013. The cyclic GMP-dependent protein kinase Ialpha suppresses kidney fibrosis |pdf=|usr=}}{{23760283}} gab.com Text The cyclic GMP-dependent protein kinase Ialpha suppresses kidney fibrosis JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=23760283 #FOAvip Cyclic guanosine monophosphate (cGMP) is synthesized by nitric oxide or natriuretic peptide-stimulated guanylyl cyclases and exhibits pleiotropic regulatory functions in the kidney. Hence, integration of cGMP signaling by cGMP-dependent protein kinases (cGKs) might play a critical role in renal physiology; however, detailed renal localization of cGKs is still lacking. Here, we performed an immunohistochemical analysis of cGKIalpha and cGKIbeta isozymes in the mouse kidney and found both in arterioles, the mesangium, and within the cortical interstitium. In contrast to cGKIalpha, the beta-isoform was not detected in the juxtaglomerular apparatus or medullary fibroblasts. Since interstitial fibroblasts play a prominent role in interstitial fibrosis, we focused our study on cGKI function in the interstitium, emphasizing a functional differentiation of both isoforms, and determined whether cGKIs influence renal fibrosis induced by unilateral ureter obstruction. Treatment with the guanylyl cyclase activators YC1 or isosorbide dinitrate showed stronger antifibrotic effects in wild-type than in cGKI-knockout or in smooth muscle-cGKIalpha-rescue mice, which are cGKI deficient in the kidney except in the renal vasculature. Moreover, fibrosis influenced the mRNA and protein expression levels of cGKIalpha more strongly than cGKIbeta. Thus, our results indicate that cGMP, acting primarily through cGKIalpha, is an important suppressor of kidney fibrosis. Twit Text FOAVip The cyclic GMP-dependent protein kinase Ialpha suppresses kidney fibrosis ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=23760283 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23760283 #FOAvip English Wikipedia <ref>{{Cite pmid|23760283}}</ref> The cyclic GMP-dependent protein kinase Ialpha suppresses kidney fibrosis #MMPMID23760283 Schinner E; Schramm A; Kees F; Hofmann F; Schlossmann J Kidney Int 2013[Dec]; 84 (6): 1198-206 PMID23760283show ga Cyclic guanosine monophosphate (cGMP) is synthesized by nitric oxide or natriuretic peptide-stimulated guanylyl cyclases and exhibits pleiotropic regulatory functions in the kidney. Hence, integration of cGMP signaling by cGMP-dependent protein kinases (cGKs) might play a critical role in renal physiology; however, detailed renal localization of cGKs is still lacking. Here, we performed an immunohistochemical analysis of cGKIalpha and cGKIbeta isozymes in the mouse kidney and found both in arterioles, the mesangium, and within the cortical interstitium. In contrast to cGKIalpha, the beta-isoform was not detected in the juxtaglomerular apparatus or medullary fibroblasts. Since interstitial fibroblasts play a prominent role in interstitial fibrosis, we focused our study on cGKI function in the interstitium, emphasizing a functional differentiation of both isoforms, and determined whether cGKIs influence renal fibrosis induced by unilateral ureter obstruction. Treatment with the guanylyl cyclase activators YC1 or isosorbide dinitrate showed stronger antifibrotic effects in wild-type than in cGKI-knockout or in smooth muscle-cGKIalpha-rescue mice, which are cGKI deficient in the kidney except in the renal vasculature. Moreover, fibrosis influenced the mRNA and protein expression levels of cGKIalpha more strongly than cGKIbeta. Thus, our results indicate that cGMP, acting primarily through cGKIalpha, is an important suppressor of kidney fibrosis. |Animals[MESH] |Cells, Cultured[MESH] |Collagen Type I, alpha 1 Chain[MESH] |Collagen Type I/genetics/metabolism[MESH] |Cyclic GMP-Dependent Protein Kinase Type I/deficiency/genetics/*metabolism[MESH] |Disease Models, Animal[MESH] |Enzyme Activation[MESH] |Enzyme Activators/pharmacology[MESH] |Fibroblasts/enzymology/pathology[MESH] |Fibronectins/genetics/metabolism[MESH] |Fibrosis[MESH] |Gene Expression Regulation, Enzymologic[MESH] |Guanylate Cyclase/metabolism[MESH] |Isoenzymes[MESH] |Kidney Diseases/enzymology/etiology/pathology/*prevention & control[MESH] |Kidney/drug effects/*enzymology/pathology[MESH] |Mice[MESH] |Mice, 129 Strain[MESH] |RNA, Messenger/metabolism[MESH] |S100 Calcium-Binding Protein A4[MESH] |S100 Proteins/genetics/metabolism[MESH] |Signal Transduction[MESH] |Transforming Growth Factor beta/genetics/metabolism[MESH] |Ureteral Obstruction/complications[MESH] |rho GTP-Binding Proteins/metabolism[MESH] |rho-Associated Kinases/metabolism[MESH]The cyclic GMP-dependent protein kinase Ialpha suppresses kidney fibro(epmc).pdf DeepDyve Pubget Overpricing