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10.5527/wjn.v5.i3.288 http://scihub22266oqcxt.onion/10.5527/wjn.v5.i3.288 C4848152!4848152 !27152265     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27152265 &cmd=llinks): Failed to open stream: HTTP request failed! 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C5b-9 does not mediate tubulointerstitial injury in experimental acute glomerular disease characterized by selective proteinuria |pdf=|usr=}}{{27152265 }} gab.com Text C5b-9 does not mediate tubulointerstitial injury in experimental acute glomerular disease characterized by selective proteinuria JO: World J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27152265 #FOAvip AIM: To determine whether complement membrane attack complex (C5b-9) has a pathogenic role in tubulointerstitial injury in a renal disease model characterized by acute highly selective proteinuria. METHODS: Protein-overload nephropathy (PON) was induced in adult female Piebald-Viral-Glaxo rats with or without complement C6 deficiency (C6(-) and C6(+)) by daily intraperitoneal injections of bovine serum albumin (BSA, 2 g/d), and examined on days 2, 4 and 8. RESULTS: Groups with PON developed equivalent levels of heavy proteinuria within 24 h of BSA injection. In C6(+) rats with PON, the tubulointerstitial expression of C5b-9 was increased and localized predominantly to the basolateral surface of tubular epithelial cells (TECs), whereas it was undetectable in C6(-) animals. TEC proliferation (as assessed by the number of BrdU+ cells) increased by more than 50-fold in PON, peaking on day 2 and declining on days 4 to 8. There was a trend for a reduction in the number of BrdU+ TECs on day 4 in the C6(-) PON group (P = 0.10 compared to C6(+)) but not at any other time-point. Kidney enlargement, TEC apoptosis (TUNEL(+) cells) and markers of tubular injury (tubule dilatation, loss of TEC height, protein cast formation) were not altered by C6 deficiency in PON. Interstitial monocyte (ED-1+ cell) accumulation was partially reduced in C6(-) animals with PON on day 4 (P = 0.01) but there was no change in myofibroblast accumulation. CONCLUSION: These data suggest that C5b-9 does not mediate tubulointerstitial injury in acute glomerular diseases characterized by selective proteinuria. Twit Text FOAVip C5b-9 does not mediate tubulointerstitial injury in experimental acute glomerular disease characterized by selective proteinuria ????World J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27152265 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27152265 #FOAvip English Wikipedia <ref>{{Cite pmid|27152265 }}</ref> C5b-9 does not mediate tubulointerstitial injury in experimental acute glomerular disease characterized by selective proteinuria #MMPMID27152265 Rangan GK World J Nephrol 2016[May]; 5 (3 ): 288-99 PMID27152265 show ga AIM: To determine whether complement membrane attack complex (C5b-9) has a pathogenic role in tubulointerstitial injury in a renal disease model characterized by acute highly selective proteinuria. METHODS: Protein-overload nephropathy (PON) was induced in adult female Piebald-Viral-Glaxo rats with or without complement C6 deficiency (C6(-) and C6(+)) by daily intraperitoneal injections of bovine serum albumin (BSA, 2 g/d), and examined on days 2, 4 and 8. RESULTS: Groups with PON developed equivalent levels of heavy proteinuria within 24 h of BSA injection. In C6(+) rats with PON, the tubulointerstitial expression of C5b-9 was increased and localized predominantly to the basolateral surface of tubular epithelial cells (TECs), whereas it was undetectable in C6(-) animals. TEC proliferation (as assessed by the number of BrdU+ cells) increased by more than 50-fold in PON, peaking on day 2 and declining on days 4 to 8. There was a trend for a reduction in the number of BrdU+ TECs on day 4 in the C6(-) PON group (P = 0.10 compared to C6(+)) but not at any other time-point. Kidney enlargement, TEC apoptosis (TUNEL(+) cells) and markers of tubular injury (tubule dilatation, loss of TEC height, protein cast formation) were not altered by C6 deficiency in PON. Interstitial monocyte (ED-1+ cell) accumulation was partially reduced in C6(-) animals with PON on day 4 (P = 0.01) but there was no change in myofibroblast accumulation. CONCLUSION: These data suggest that C5b-9 does not mediate tubulointerstitial injury in acute glomerular diseases characterized by selective proteinuria. äC5b-9 does not mediate tubulointerstitial injury in experimental acute(epmc).pdf DeepDyve Pubget Overpricing