BACKGROUND/AIMS: 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. CONCLUSION: The injured glomerular epithelial cells in anti-GBM nephritis might undergo structural and functional alterations, including the expression of a smooth muscle marker, SM22alpha. Copyright 2007 S. Karger AG, Basel.
BACKGROUND/AIMS: 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 ratSM22alpha 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. CONCLUSION: The injured glomerular epithelial cells in anti-GBM nephritis might undergo structural and functional alterations, including the expression of a smooth muscle marker, SM22alpha. Copyright 2007 S. Karger AG, Basel.
Authors: Caroline B Marshall; Ron D Krofft; Mary J Blonski; Jolanta Kowalewska; Christine M Logar; Jeffrey W Pippin; Francis Kim; Robert Feil; Charles E Alpers; Stuart J Shankland Journal: Am J Physiol Renal Physiol Date: 2011-02-02
Authors: Erika K Wells; OrLando Yarborough; Richard P Lifton; Lloyd G Cantley; Michael J Caplan Journal: Am J Physiol Cell Physiol Date: 2013-03-13 Impact factor: 4.249
Authors: Hui-Min Zhou; Yuan-Yuan Fang; Paul M Weinberger; Ling-Ling Ding; John K Cowell; Farlyn Z Hudson; Mingqiang Ren; Jeffrey R Lee; Qi-Kui Chen; Hong Su; William S Dynan; Ying Lin Journal: BMC Cancer Date: 2016-02-04 Impact factor: 4.430