title: Renal lymphatic ligation aggravates renal dysfunction through induction of tubular epithelial cell apoptosis in mononephrectomized rats.
abstract: OBJECTIVE
  To further explore the mechanisms of apoptosis in mononephrectomized rats with renal lymph circulation disorder.
  
  
  METHODS
  Animals were divided into three groups: rats with left renal lymph ligation and right nephrectomy (KL), rats with only right nephrectomy (KN) and sham-operated rats (sham). 24-h proteinuria and serum creatinine level were monitored. Indexes of oxidative stress were measured. Renal apoptosis was examined. Further biochemical analysis was provided using real-time PCR, western blot and Elisa techniques.
  
  
  RESULTS
  Our results showed that renal lymphatic ligation induced renal tubular epithelial cell apoptosis and aggravated renal dysfunction in mononephrectomized rats. In addition, renal lymphatic ligation increased the activities of caspase-3, caspase-8 and caspase-9. Further investigation of mechanisms showed that renal lymphatic ligation up-regulated Fas expression, increased the ratio of Bax/Bcl-2, and also increased the levels of reactive oxygen species (ROS), malondialdehyde (MDA) while reducing superoxide dismutase (SOD) activity.
  
  
  CONCLUSIONS
  These results indicated that disturbance of renal lymphatic circulation might lead to tubular epithelial cell apoptosis through activation of intrinsic and extrinsic apoptotic pathways, suggestive of an essential role of renal lymphatic circulation in the maintenance of tubular integrity and function.
authors.affiliation: Department of Nephrology, the second affiliated hospital of Shandong University, Jinan, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Cheng
authors.forename: Jianping
authors.initials: J
authors.lastname: Wang
authors.forename: Yuan-tao
authors.initials: YT
authors.lastname: Liu
authors.forename: Taoyan
authors.initials: T
authors.lastname: Zhang
authors.forename: Aili
authors.initials: A
authors.lastname: Sun
authors.forename: Weiwei
authors.initials: W
authors.lastname: Wang
authors.forename: Shasha
authors.initials: S
authors.lastname: Lv
authors.forename: Shanshan
authors.initials: S
authors.lastname: Liu
authors.forename: Guangju
authors.initials: G
authors.lastname: Guan
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D020169:Caspases / Q000032:analysis / Q000378:metabolism; D053222:Fas Ligand Protein / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D006651:Histocytochemistry; D007668:Kidney / Q000737:chemistry / Q000293:injuries* / Q000378:metabolism / Q000502:physiology; D007674:Kidney Diseases / Q000503:physiopathology*; D007684:Kidney Tubules / Q000473:pathology* / Q000503:physiopathology; D008026:Ligation / Q000379:methods; D042601:Lymphatic Vessels / Q000293:injuries* / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000378:metabolism; D009392:Nephrectomy; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000032:analysis / Q000378:metabolism; D013482:Superoxide Dismutase / Q000032:analysis / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000032:analysis / Q000235:genetics / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D053222:Fas Ligand Protein; C505662:Faslg protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D020169:Caspases