SM22α:: the novel phenotype marker of injured glomerular epithelial cells in anti-glomerular basement membrane nephritis

Background/Aims: Our previous comprehensive analysis of the genes expressed in kidneys with anti-glomerular basement membrane ( GBM) nephritis using DNA microarrays showed that SM22 alpha was one of the highly expressed genes. SM22 alpha is a 22-kDa cytoskeletal protein that is exclusively expressed in smooth muscle cells. We investigated the localization of SM22 alpha 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 SM22 alpha was obtained by immunization of rabbits with recombinant rat SM22 alpha protein. Results: SM22 alpha mRNA expression was up-regulated in kidneys and inducibly expressed in the parietal and visceral glomerular epithelial cells in anti-GBM nephritis kidneys. Immunohistochemistry with anti-SM22 alpha Ab showed that SM22 alpha protein was localized in the same series of cells. Double immunofluorescence with anti-SM22 alpha and anti- glomerular cell markers demonstrated that SM22 alpha might be expressed in epithelial cells of injured glomeruli. In visceral epithelial cells, SM22 alpha might be expressed in cells in which podocyte specific markers, podocalyxin and nephrin were lost. Conclusion: The injured glomerular epithelial cells in anti-GBM nephritis might undergo structural and functional alterations, including the expression of a smooth muscle marker, SM22 alpha. Copyright (C) 2007 S. Karger AG, Basel.