title: Comparative Proteomics Analysis of Mouse Habu Nephritis Models with and without Unilateral Nephrectomy.
abstract: OBJECTIVE
  Individuals possessing a single kidney are at greater risk of renal injury upon exposure to harmful stimuli. This study aimed to explore the pathogenesis of renal injury in glomerulonephritis with versus without unilateral nephrectomy (UNX).
  
  
  METHODS
  Histological analysis and label-free quantitative proteomics were performed on two models-the Habu snake venom-induced glomerulonephritis model with versus without UNX (HabuU and Habu models, respectively). The role of villin 1, a differentially expressed protein (DEP) in mouse mesangial cells, was investigated.
  
  
  RESULTS
  Persistent mesangiolysis and focal hypercellularity together with reduced activation of cell proliferation in the HabuU model induced more serious renal injury compared with that in the Habu model. The DEPs between the two models were identified by label-free liquid chromatography-mass spectrometry. The KEGG pathway results indicated that regulation of actin cytoskeleton and focal adhesion were specifically enriched in the HabuU model. The cytoskeleton regulation protein villin 1 was downregulated in the HabuU model, but unchanged in the Habu model. Knockdown of villin 1 promoted apoptosis and inhibited the proliferation of mouse mesangial cells, suggesting villin 1 to be involved in qlomerular lesion self-repair insufficiency.
  
  
  CONCLUSIONS
  By assessing the proteomic profiles of the two models, this study identified several important differences, particularly villin 1 expression, in regulatory mechanisms between the two models. Our findings provide novel insight into the mechanism of serious renal injury in glomerulonephritis with UNX.
authors.affiliation: Dialysis Department of Nephrology Hospital, First Affiliated Hospital of Medicine School, Xi'an Jiaotong University, Xi'an, People's Republic of China.
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Yang
authors.initials: Y
authors.lastname: Lu
authors.forename: Jun
authors.initials: J
authors.lastname: Wen
authors.forename: Xu
authors.initials: X
authors.lastname: Wang
authors.forename: Lingling
authors.initials: L
authors.lastname: Wu
authors.forename: Di
authors.initials: D
authors.lastname: Wu
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Sun
authors.forename: Bo
authors.initials: B
authors.lastname: Fu
authors.forename: Zhong
authors.initials: Z
authors.lastname: Yin
authors.forename: Hongli
authors.initials: H
authors.lastname: Jiang
authors.forename: Xiangmei
authors.initials: X
authors.lastname: Chen
mesh_terms: D008841:Actin Cytoskeleton / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D004195:Disease Models, Animal; D022001:Focal Adhesions / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D005920:Glomerular Mesangium / Q000187:drug effects / Q000378:metabolism* / Q000601:surgery / Q000648:ultrastructure; D005921:Glomerulonephritis / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology / Q000601:surgery; D006801:Humans; D008297:Male; D050527:Mesangial Cells / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D051379:Mice; D008810:Mice, Inbred C57BL; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism; D058977:Molecular Sequence Annotation; D009392:Nephrectomy; D061251:Primary Cell Culture; D040901:Proteomics; D012910:Snake Venoms / Q000633:toxicity*
chemical_list: D008840:Microfilament Proteins; D012910:Snake Venoms; C026615:villin