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      SM22α: The Novel Phenotype Marker of Injured Glomerular Epithelial Cells in Anti-Glomerular Basement Membrane Nephritis

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          Background/Aims: Our previous comprehensive analysis of the genes expressed in kidneys with anti-glomerular basement membrane (GBM) nephritis using DNA microarrays showed that SM22α was one of the highly expressed genes. SM22α is a 22-kDa cytoskeletal protein that is exclusively expressed in smooth muscle cells. We investigated the localization of SM22α 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 SM22α was obtained by immunization of rabbits with recombinant rat SM22α protein. Results: SM22α 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-SM22α Ab showed that SM22α protein was localized in the same series of cells. Double immunofluorescence with anti-SM22α and anti-glomerular cell markers demonstrated that SM22α might be expressed in epithelial cells of injured glomeruli. In visceral epithelial cells, SM22α 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, SM22α.

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          Most cited references 27

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          Podocyte biology and response to injury.

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            SM22alpha modulates vascular smooth muscle cell phenotype during atherogenesis.

            The function of cytoskeletal proteins in the modulation of vascular smooth muscle cell (SMC) phenotype during vascular disease is poorly understood. In this report, we used a combination of gene targeting and Cre/lox-mediated cell fate mapping in mice to investigate the role of SM22alpha, an SMC-specific cytoskeletal protein of unknown function, in the development of atherosclerosis. In hypercholesterolemic ApoE-deficient mice, genetic ablation of SM22alpha resulted in increased atherosclerotic lesion area and a higher proportion of proliferating SMC-derived plaque cells. These results identify a role for SM22alpha in the regulation of SMC phenotype during atherogenesis.
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              Calponin and SM 22 as differentiation markers of smooth muscle: spatiotemporal distribution during avian embryonic development.

              Calponin and SM 22 are two proteins related in sequence that are particularly abundant in smooth muscle cells. Here, the distribution patterns of calponin and SM 22 were compared with that of other smooth muscle contractile and cytoskeletal components in the avian embryo using immunofluorescence microscopy and immunoblotting. Like myosin-light-chain kinase and heavy caldesmon, both calponin and SM 22 were more or less exclusively found in smooth muscle cells, during embryonic development and in the adult. Labelling of other cell types including striated muscle was not observed. In contrast, tropomyosin, smooth muscle alpha-actin, filamin and desmin could also be detected in many other cell types in addition to smooth muscles, at least during part of embryonic life. Calponin and SM 22 appeared almost synchronously during the differentiation of all smooth muscle cell populations, though with a slight time difference in the case of the aorta. The appearance of calponin, SM 22 and heavy caldesmon was generally delayed in relation to desmin, tropomyosin, smooth muscle alpha-actin, myosin-light-chain kinase and filamin and a marked increase in abundance of these proteins was observed in the late embryo and in the adult. From these observations we can conclude that both calponin and SM 22 belong to a group of late differentiation determinants in smooth muscle and may constitute convenient and reliable markers to follow the differentiation of most, if not all, smooth muscle cell populations.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                July 2007
                22 May 2007
                : 106
                : 3
                : e77-e87
                aDivision of Clinical Nephrology and Rheumatology, and bDivision of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
                103020 Nephron Exp Nephrol 2007;106:e77–e87
                © 2007 S. Karger AG, Basel

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                Figures: 9, References: 38, Pages: 1
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