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10.1152/ajprenal.00444.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00444.2014 C4398838!4398838 !25673808     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25673808 &cmd=llinks): Failed to open stream: HTTP request failed! 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Unilateral ureteral obstruction attenuates intrarenal angiotensin II generation induced by podocyte injury |pdf=|usr=}}{{25673808 }} gab.com Text Unilateral ureteral obstruction attenuates intrarenal angiotensin II generation induced by podocyte injury JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25673808 #FOAvip The renal tissue renin-angiotensin system is activated in chronic kidney diseases. We previously demonstrated that intrarenal ANG II is synthesized primarily from liver-derived angiotensinogen filtered through the glomerulus and that podocyte injury increases the passage of angiotensinogen into the tubular lumen and generation of ANG II. In the present study, we tested the effect of cessation of glomerular filtration by ureteral obstruction on renal ANG II generation in kidneys with podocyte injury under two experimental conditions. Ureteral obstruction is known to activate the renin-angiotensin system in nonproteinuric kidneys. Transgenic mice expressing hCD25 in podocyte (NEP25) were injected with 1.25 or 10 ng/g body wt of LMB2, a hCD25-targeted immunotoxin, subjected to unilateral ureteral ligation on the following day, and euthanized 7 and 4 days later, respectively. In both experiments, compared with the kidney in untreated wild-type mice, renal angiotensinogen protein, as assessed by immunostaining and Western blot analysis, was increased in the contralateral unobstructed kidney. However, it was markedly decreased in the obstructed kidney. Whereas intrarenal ANG II content was increased in the contralateral kidney compared with the untreated kidney (248 ± 83 vs. 106 ± 21 and 298 ± 185 vs. 64.8 ± 20 fmol/g kidney, respectively), this increase was suppressed in the obstructed kidney (161 ± 75 and 113 ± 34 fmol/g kidney, respectively), a pattern opposite to what we expected in obstructed kidneys without podocyte injury. Thus, our study indicates that the major source of increased renal ANG II in podocyte injury is filtered angiotensinogen. Twit Text FOAVip Unilateral ureteral obstruction attenuates intrarenal angiotensin II generation induced by podocyte injury ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25673808 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25673808 #FOAvip English Wikipedia <ref>{{Cite pmid|25673808 }}</ref> Unilateral ureteral obstruction attenuates intrarenal angiotensin II generation induced by podocyte injury #MMPMID25673808 Okabe M ; Miyazaki Y ; Niimura F ; Pastan I ; Nishiyama A ; Yokoo T ; Ichikawa I ; Matsusaka T Am J Physiol Renal Physiol 2015[Apr]; 308 (8 ): F932-7 PMID25673808 show ga The renal tissue renin-angiotensin system is activated in chronic kidney diseases. We previously demonstrated that intrarenal ANG II is synthesized primarily from liver-derived angiotensinogen filtered through the glomerulus and that podocyte injury increases the passage of angiotensinogen into the tubular lumen and generation of ANG II. In the present study, we tested the effect of cessation of glomerular filtration by ureteral obstruction on renal ANG II generation in kidneys with podocyte injury under two experimental conditions. Ureteral obstruction is known to activate the renin-angiotensin system in nonproteinuric kidneys. Transgenic mice expressing hCD25 in podocyte (NEP25) were injected with 1.25 or 10 ng/g body wt of LMB2, a hCD25-targeted immunotoxin, subjected to unilateral ureteral ligation on the following day, and euthanized 7 and 4 days later, respectively. In both experiments, compared with the kidney in untreated wild-type mice, renal angiotensinogen protein, as assessed by immunostaining and Western blot analysis, was increased in the contralateral unobstructed kidney. However, it was markedly decreased in the obstructed kidney. Whereas intrarenal ANG II content was increased in the contralateral kidney compared with the untreated kidney (248 ± 83 vs. 106 ± 21 and 298 ± 185 vs. 64.8 ± 20 fmol/g kidney, respectively), this increase was suppressed in the obstructed kidney (161 ± 75 and 113 ± 34 fmol/g kidney, respectively), a pattern opposite to what we expected in obstructed kidneys without podocyte injury. Thus, our study indicates that the major source of increased renal ANG II in podocyte injury is filtered angiotensinogen. |*Renin-Angiotensin System/genetics [MESH] |Albuminuria/metabolism/pathology/physiopathology [MESH] |Angiotensin II/*metabolism [MESH] |Angiotensinogen/genetics/*metabolism [MESH] |Animals [MESH] |Antibodies, Monoclonal [MESH] |Disease Models, Animal [MESH] |Down-Regulation [MESH] |Exotoxins [MESH] |Female [MESH] |Glomerular Filtration Rate [MESH] |Humans [MESH] |Interleukin-2 Receptor alpha Subunit/genetics/metabolism [MESH] |Kidney Diseases/chemically induced/genetics/*metabolism/pathology/physiopathology [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Podocytes/*metabolism/pathology [MESH] |RNA, Messenger/metabolism [MESH] |Signal Transduction [MESH] |Time Factors [MESH]Unilateral ureteral obstruction attenuates intrarenal angiotensin II g(epmc).pdf DeepDyve Pubget Overpricing