{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,19]],"date-time":"2024-05-19T09:27:01Z","timestamp":1716110821144},"reference-count":39,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:p>Obstructive kidney disease is a common complication in the clinic. Downregulation of aquaporins (AQPs) in obstructed kidneys has been thought as a key factor leading to the polyuria and impairment of urine-concentrating capability after the release of kidney obstruction. The present study was to investigate the role of mitochondrial complex-1 in modulating AQPs in obstructive nephropathy. Following 7-day unilateral ureteral obstruction (UUO), AQP1, AQP2, AQP3, and vasopressin 2 (V<jats:sub>2<\/jats:sub>) receptor were remarkably reduced as determined by qRT-PCR and\/or Western blotting. Notably, inhibition of mitochondrial complex-1 by rotenone markedly reversed the downregulation of AQP1, AQP2, AQP3, and V<jats:sub>2<\/jats:sub>. In contrast, AQP4 was not affected by kidney obstruction or rotenone treatment. In a separate study, rotenone also attenuated AQPs' downregulation after 48-h UUO. To study the potential mechanisms in mediating the rotenone effects on AQPs, we examined the regulation of the COX-2\/microsomal prostaglandin E synthase (mPGES)-1\/PGE<jats:sub>2<\/jats:sub>\/EP pathway and found that COX-2, mPGES-1, and renal PGE<jats:sub>2<\/jats:sub>content were all significantly elevated in obstructive kidneys, which was not affected by rotenone treatment. For EP receptors, EP<jats:sub>2<\/jats:sub>and EP<jats:sub>4<\/jats:sub>but not EP<jats:sub>1<\/jats:sub>and EP<jats:sub>3<\/jats:sub>were upregulated in obstructive kidneys. Importantly, rotenone strikingly suppressed EP<jats:sub>1<\/jats:sub>and EP<jats:sub>4<\/jats:sub>but not EP<jats:sub>2<\/jats:sub>and EP<jats:sub>3<\/jats:sub>receptors. However, treatment of EP<jats:sub>1<\/jats:sub>antagonist SC-51322 could not affect AQPs' reduction in obstructed kidneys. Collectively, these findings suggested an important role of mitochondrial dysfunction in modulating AQPs and V<jats:sub>2<\/jats:sub>receptor in obstructive nephropathy possibly via prostaglandin-independent mechanisms.<\/jats:p>","DOI":"10.1152\/ajprenal.00215.2015","type":"journal-article","created":{"date-parts":[[2016,7,14]],"date-time":"2016-07-14T06:37:07Z","timestamp":1468478227000},"page":"F777-F786","source":"Crossref","is-referenced-by-count":14,"title":["Inhibition of mitochondrial complex-1 restores the downregulation of aquaporins in obstructive nephropathy"],"prefix":"10.1152","volume":"311","author":[{"given":"Ying","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Nephrology, Nanjing Children's Hospital, Affiliated to Nanjing Medical University, Nanjing, China;"},{"name":"Department of Pharmacy, Xuzhou Medical University, Xuzhou, China;"},{"name":"Nanjing Key Laboratory of Pediatric, Nanjing Children Hospital, Affiliated to Nanjing Medical 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