title: The role of autophagy in unilateral ureteral obstruction rat model.
abstract: OBJECTIVE
  Autophagy is a cellular process of degradation of damaged cytoplasmic components and regulates cell death or proliferation. Unilateral ureteral obstruction (UUO) is a model of progressive renal fibrosis in the obstructed kidney. And UUO is followed by compensatory cellular proliferation in the contralateral kidney. We investigate the role of autophagy in the obstructed kidney and contralateral kidney after UUO.
  
  
  METHODS
  To obtain the evidence and the patterns of autophagy during UUO, the rats were sacrificed 3, 7 and 14 days after UUO. To examine the efficacy of the autophagy inhibitors, 3-methyladenine (3-MA), the rats were treated daily with intraperitoneal injection of 3-MA (30 mg/kg per day) for 7 days.
  
  
  RESULTS
  After UUO, autophagy was induced in the obstructed kidney in a time-dependent manner. Inhibition of autophagy by 3-MA enhanced tubular cell apoptosis and tubulointerstitial fibrosis in the obstructed kidney after UUO. In the contralateral kidney, autophagy was also induced and prolonged during UUO. Inhibition of autophagy by 3-MA increased the protein expression of proliferating cell nuclear antigen significantly in the contralateral kidney after UUO. The Akt-mammalian target of rapamycin (mTOR) signalling pathway was involved in the induction of autophagy after UUO in both kidneys.
  
  
  CONCLUSIONS
  Our present results support that autophagy induced by UUO has a renoprotective role in the obstructed kidney and regulatory role of compensatory cellular proliferation in the contralateral kidney through Akt-mTOR signalling pathway.
authors.affiliation: Department of Anatomy and MRC for Cell Death Disease Research Center, Bucheon Saint Mary’s Hospital, Sosa-dong, Wonmi-gu, Bucheon-si, Geoynggi-do, 420-717 Korea.
authors.forename: Wan-Young
authors.initials: WY
authors.lastname: Kim
authors.forename: Sun Ah
authors.initials: SA
authors.lastname: Nam
authors.forename: Ho Cheol
authors.initials: HC
authors.lastname: Song
authors.forename: Jun Sung
authors.initials: JS
authors.lastname: Ko
authors.forename: Sang Hee
authors.initials: SH
authors.lastname: Park
authors.forename: Hong Lim
authors.initials: HL
authors.lastname: Kim
authors.forename: Euy Jin
authors.initials: EJ
authors.lastname: Choi
authors.forename: Yong-Soo
authors.initials: YS
authors.lastname: Kim
authors.forename: Jin
authors.initials: J
authors.lastname: Kim
authors.forename: Yong Kyun
authors.initials: YK
authors.lastname: Kim
mesh_terms: D000225:Adenine / Q000008:administration & dosage / Q000031:analogs & derivatives; D000818:Animals; D017209:Apoptosis; D001343:Autophagy / Q000187:drug effects; D049109:Cell Proliferation; D019610:Cytoprotection; D004195:Disease Models, Animal; D005355:Fibrosis; D007274:Injections, Intraperitoneal; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D013997:Time Factors; D014517:Ureteral Obstruction / Q000378:metabolism / Q000473:pathology*
chemical_list: D018809:Proliferating Cell Nuclear Antigen; C025946:3-methyladenine; C546845:mTOR protein, rat; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D000225:Adenine