title: SM22alpha: the novel phenotype marker of injured glomerular epithelial cells in anti-glomerular basement membrane nephritis.
abstract: OBJECTIVE
  Our previous comprehensive analysis of the genes expressed in kidneys with anti-glomerular basement membrane (GBM) nephritis using DNA microarrays showed that SM22alpha was one of the highly expressed genes. SM22alpha is a 22-kDa cytoskeletal protein that is exclusively expressed in smooth muscle cells. We investigated the localization of SM22alpha at mRNA and protein levels, and its pathological significance in anti-GBM nephritis kidneys.
  
  
  METHODS
  Northern blot analysis, in situ hybridization, immunohistochemistry and double immunofluorescence studies were performed. The specific antibody (Ab) against SM22alpha was obtained by immunization of rabbits with recombinant rat SM22alpha protein.
  
  
  RESULTS
  SM22alpha mRNA expression was upregulated in kidneys and inducibly expressed in the parietal and visceral glomerular epithelial cells in anti-GBM nephritis kidneys. Immunohistochemistry with anti-SM22alpha Ab showed that SM22alpha protein was localized in the same series of cells. Double immunofluorescence with anti-SM22alpha and anti-glomerular cell markers demonstrated that SM22alpha might be expressed in epithelial cells of injured glomeruli. In visceral epithelial cells, SM22alpha might be expressed in cells in which podocyte specific markers, podocalyxin and nephrin were lost.
  
  
  CONCLUSIONS
  The injured glomerular epithelial cells in anti-GBM nephritis might undergo structural and functional alterations, including the expression of a smooth muscle marker, SM22alpha.
authors.affiliation: Division of Clinical Nephrology and Rheumatology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Asa
authors.initials: A
authors.lastname: Ogawa
authors.forename: Minoru
authors.initials: M
authors.lastname: Sakatsume
authors.forename: Xingzhi
authors.initials: X
authors.lastname: Wang
authors.forename: Yunichi
authors.initials: Y
authors.lastname: Sakamaki
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Tsubata
authors.forename: Bassam
authors.initials: B
authors.lastname: Alchi
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kuroda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kawachi
authors.forename: Ichiei
authors.initials: I
authors.lastname: Narita
authors.forename: Fujio
authors.initials: F
authors.lastname: Shimizu
authors.forename: Fumitake
authors.initials: F
authors.lastname: Gejyo
mesh_terms: D000818:Animals; D001485:Basement Membrane / Q000276:immunology*; D015415:Biomarkers / Q000378:metabolism; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation; D005921:Glomerulonephritis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D007074:Immunoglobulin G; D007678:Kidney Glomerulus / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism*; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D011921:Rats, Inbred WKY; D012795:Sialoglycoproteins / Q000235:genetics / Q000378:metabolism
chemical_list: D015415:Biomarkers; D007074:Immunoglobulin G; D008565:Membrane Proteins; D008840:Microfilament Proteins; D009124:Muscle Proteins; D012333:RNA, Messenger; D012795:Sialoglycoproteins; C113267:nephrin; C001643:podocalyxin; C051615:transgelin