title: Injured kidney cells express SM22α (transgelin): Unique features distinct from α-smooth muscle actin (αSMA).
abstract: OBJECTIVE
  SM22α (transgelin) has been focused upon as a player in the process of phenotypic changes of types of cells. The SM22α expression in the rat anti-glomerular basement membrane (GBM) nephritis model and differences from an established phenotypic marker for the myofibroblast, α-smooth muscle actin (αSMA), were investigated.
  
  
  METHODS
  The rat kidney tissues were processed for histological studies, immunohistochemical and immunoelectronmicroscopy analyses on days 0, 7, 28, 42 and 56 after injection of rabbit anti-GBM serum for the disease induction.
  
  
  RESULTS
  Immunohistochemistry with anti-SM22α antibodies (Ab) revealed that kidneys of the nephritic rats on day 7 expressed SM22α in podocytes, crescentic cells and epithelial cells of Bowman's capsule. After 28 days, SM22α was also expressed in peritubular interstitial cells. Double immunofluorescence with anti-SM22α Ab and anti-αSMA Ab showed that SM22α was preferentially expressed in podocytes, whereas αSMA was positive in mesangial cells on day 7. After day 28, both molecules became positive in peritubular interstitial cells.
  
  
  CONCLUSIONS
  SM22α was expressed in epithelial cells of inflamed glomeruli in the early phase, and then also in peritubular interstitial cells in the later phase of anti-GBM nephritis model. SM22α presented unique kinetics of expression distinct from αSMA.
authors.affiliation: Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Sakamaki
authors.forename: Minoru
authors.initials: M
authors.lastname: Sakatsume
authors.forename: Xingzhi
authors.initials: X
authors.lastname: Wang
authors.forename: Shigeru
authors.initials: S
authors.lastname: Inomata
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Fumitake
authors.initials: F
authors.lastname: Gejyo
authors.forename: Ichiei
authors.initials: I
authors.lastname: Narita
mesh_terms: D000199:Actins / Q000378:metabolism*; D000818:Animals; D001485:Basement Membrane / Q000276:immunology*; D015415:Biomarkers / Q000378:metabolism; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism; D005921:Glomerulonephritis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D007074:Immunoglobulin G; D007678:Kidney Glomerulus / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism*; D009124:Muscle Proteins / Q000378:metabolism*; D050199:Podocytes / Q000378:metabolism; D051381:Rats; D011921:Rats, Inbred WKY
chemical_list: D000199:Actins; D015415:Biomarkers; D007074:Immunoglobulin G; D008840:Microfilament Proteins; D009124:Muscle Proteins; C498862:Acta2 protein, rat; C051615:transgelin