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10.1093/toxsci/kfv038 http://scihub22266oqcxt.onion/10.1093/toxsci/kfv038 C4408963!4408963!25666834     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25666834&cmd=llinks): Failed to open stream: HTTP request failed! 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Urinary ATP Synthase Subunit ? Is a Novel Biomarker of Renal Mitochondrial Dysfunction in Acute Kidney Injury |pdf=|usr=}}{{25666834}} gab.com Text Urinary ATP Synthase Subunit Is a Novel Biomarker of Renal Mitochondrial Dysfunction in Acute Kidney Injury JO: Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25666834 #FOAvip Although the importance of mitochondrial dysfunction in acute kidney injury (AKI) has been documented, noninvasive early biomarkers of mitochondrial damage are needed. We examined urinary ATP synthase subunit ? (ATPS?) as a biomarker of renal mitochondrial dysfunction during AKI. Mice underwent sham surgery or varying degrees (5, 10, or 15?min ischemia) of ischemia/reperfusion (I/R)-induced AKI. Serum creatinine, BUN, and neutrophil gelatinase-associated lipocalin were elevated only in the 15?min I/R group at 24?h. Immunoblot analysis of urinary ATPS? revealed two bands (full length ?52?kDa and cleaved ?25?kDa), both confirmed as ATPS? by LC-MS/MS, that increased at 24?h in 10- and 15-min I/R groups. These changes were associated with mitochondrial dysfunction evidenced by reduced renal cortical expression of mitochondrial proteins, ATPS? and COX1, proximal tubular oxygen consumption, and ATP. Furthermore, in the 15-min I/R group, urinary ATPS? was elevated until 72?h before returning to baseline 144?h after reperfusion with recovery of renal function. Evaluation of urinary ATPS? in a nonalcoholic steatohepatitis model of liver injury only revealed cleaved ATPS?, suggesting specificity of full-length ATPS? for renal injury. Immunoblot analyses of patient urine samples collected 36?h after cardiac surgery revealed increased urinary ATPS? levels in patients with postcardiac surgery-induced AKI. LC-MS/MS urinalysis in human subjects with AKI confirmed increased ATPS?. These translational studies provide evidence that ATPS? may be a novel and sensitive urinary biomarker of renal mitochondrial dysfunction and could serve as valuable tool for the testing of potential therapies for AKI and chemical-induced nephrotoxicity. Twit Text FOAVip Urinary ATP Synthase Subunit Is a Novel Biomarker of Renal Mitochondrial Dysfunction in Acute Kidney Injury ????Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25666834 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25666834 #FOAvip English Wikipedia <ref>{{Cite pmid|25666834}}</ref> Urinary ATP Synthase Subunit ? Is a Novel Biomarker of Renal Mitochondrial Dysfunction in Acute Kidney Injury #MMPMID25666834 Whitaker RM; Korrapati MC; Stallons LJ; Jesinkey SR; Arthur JM; Beeson CC; Zhong Z; Schnellmann RG Toxicol Sci 2015[May]; 145 (1): 108-17 PMID25666834show ga Although the importance of mitochondrial dysfunction in acute kidney injury (AKI) has been documented, noninvasive early biomarkers of mitochondrial damage are needed. We examined urinary ATP synthase subunit ? (ATPS?) as a biomarker of renal mitochondrial dysfunction during AKI. Mice underwent sham surgery or varying degrees (5, 10, or 15?min ischemia) of ischemia/reperfusion (I/R)-induced AKI. Serum creatinine, BUN, and neutrophil gelatinase-associated lipocalin were elevated only in the 15?min I/R group at 24?h. Immunoblot analysis of urinary ATPS? revealed two bands (full length ?52?kDa and cleaved ?25?kDa), both confirmed as ATPS? by LC-MS/MS, that increased at 24?h in 10- and 15-min I/R groups. These changes were associated with mitochondrial dysfunction evidenced by reduced renal cortical expression of mitochondrial proteins, ATPS? and COX1, proximal tubular oxygen consumption, and ATP. Furthermore, in the 15-min I/R group, urinary ATPS? was elevated until 72?h before returning to baseline 144?h after reperfusion with recovery of renal function. Evaluation of urinary ATPS? in a nonalcoholic steatohepatitis model of liver injury only revealed cleaved ATPS?, suggesting specificity of full-length ATPS? for renal injury. Immunoblot analyses of patient urine samples collected 36?h after cardiac surgery revealed increased urinary ATPS? levels in patients with postcardiac surgery-induced AKI. LC-MS/MS urinalysis in human subjects with AKI confirmed increased ATPS?. These translational studies provide evidence that ATPS? may be a novel and sensitive urinary biomarker of renal mitochondrial dysfunction and could serve as valuable tool for the testing of potential therapies for AKI and chemical-induced nephrotoxicity. �Urinary ATP Synthase Subunit ? Is a Novel Biomarker of Renal Mitochond(epmc).pdf DeepDyve Pubget Overpricing