{"title":"阿霉素诱导局灶节段性肾小球硬化模型中SM22α (transgelin)的定量组织学分析。","authors":"Xingzhi Wang, Minoru Sakatsume, Yuichi Sakamaki, Shigeru Inomata, Tadashi Yamamoto, Ichiei Narita","doi":"10.1159/000329664","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/aims: </strong>SM22α, transgelin, has been revealed to be specifically expressed in glomerular epithelial cells and interstitial cells, according to the nature of the renal injury. In this study, quantitative analyses of SM22α positivity were performed to investigate the pathological significance of its expression.</p><p><strong>Methods: </strong>Kidney samples of adriamycin nephropathy underwent immunohistochemistry with a newly established anti-SM22α monoclonal antibody. The SM22α positivity was quantified by an image analyzer. The correlation of the histological values with biochemical data was investigated statistically. Microstructural localization of SM22α was studied by immunoelectron microscopy.</p><p><strong>Results: </strong>SM22α was expressed along the dense basal microfilaments of degenerating podocytes, and diffusely in interstitial cells. Both the extent and intensity of SM22α expression in glomerular and tubulointerstitial area were correlated with the deterioration of renal function and the severity of proteinuria. Stepwise multiple linear regression analysis revealed that the extent of its positivity in glomerular or tubulointerstitial area was the determinant of the amount of proteinuria or the deterioration of creatinine clearance (Ccr), respectively. Inversely, the deterioration of Ccr was the most important predictor of SM22α expression.</p><p><strong>Conclusion: </strong>SM22α expression in podocytes and interstitial cells represented the severity of proteinuria and the deterioration of renal function. SM22α expression in renal tissues might be a hallmark of kidney diseases.</p>","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"120 1","pages":"e1-11"},"PeriodicalIF":0.0000,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000329664","citationCount":"4","resultStr":"{\"title\":\"Quantitative histological analysis of SM22α (transgelin) in an adriamycin-induced focal segmental glomerulosclerosis model.\",\"authors\":\"Xingzhi Wang, Minoru Sakatsume, Yuichi Sakamaki, Shigeru Inomata, Tadashi Yamamoto, Ichiei Narita\",\"doi\":\"10.1159/000329664\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background/aims: </strong>SM22α, transgelin, has been revealed to be specifically expressed in glomerular epithelial cells and interstitial cells, according to the nature of the renal injury. In this study, quantitative analyses of SM22α positivity were performed to investigate the pathological significance of its expression.</p><p><strong>Methods: </strong>Kidney samples of adriamycin nephropathy underwent immunohistochemistry with a newly established anti-SM22α monoclonal antibody. The SM22α positivity was quantified by an image analyzer. The correlation of the histological values with biochemical data was investigated statistically. Microstructural localization of SM22α was studied by immunoelectron microscopy.</p><p><strong>Results: </strong>SM22α was expressed along the dense basal microfilaments of degenerating podocytes, and diffusely in interstitial cells. Both the extent and intensity of SM22α expression in glomerular and tubulointerstitial area were correlated with the deterioration of renal function and the severity of proteinuria. Stepwise multiple linear regression analysis revealed that the extent of its positivity in glomerular or tubulointerstitial area was the determinant of the amount of proteinuria or the deterioration of creatinine clearance (Ccr), respectively. Inversely, the deterioration of Ccr was the most important predictor of SM22α expression.</p><p><strong>Conclusion: </strong>SM22α expression in podocytes and interstitial cells represented the severity of proteinuria and the deterioration of renal function. SM22α expression in renal tissues might be a hallmark of kidney diseases.</p>\",\"PeriodicalId\":18993,\"journal\":{\"name\":\"Nephron Experimental Nephrology\",\"volume\":\"120 1\",\"pages\":\"e1-11\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000329664\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nephron Experimental Nephrology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000329664\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2011/12/23 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nephron Experimental Nephrology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000329664","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2011/12/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Quantitative histological analysis of SM22α (transgelin) in an adriamycin-induced focal segmental glomerulosclerosis model.
Background/aims: SM22α, transgelin, has been revealed to be specifically expressed in glomerular epithelial cells and interstitial cells, according to the nature of the renal injury. In this study, quantitative analyses of SM22α positivity were performed to investigate the pathological significance of its expression.
Methods: Kidney samples of adriamycin nephropathy underwent immunohistochemistry with a newly established anti-SM22α monoclonal antibody. The SM22α positivity was quantified by an image analyzer. The correlation of the histological values with biochemical data was investigated statistically. Microstructural localization of SM22α was studied by immunoelectron microscopy.
Results: SM22α was expressed along the dense basal microfilaments of degenerating podocytes, and diffusely in interstitial cells. Both the extent and intensity of SM22α expression in glomerular and tubulointerstitial area were correlated with the deterioration of renal function and the severity of proteinuria. Stepwise multiple linear regression analysis revealed that the extent of its positivity in glomerular or tubulointerstitial area was the determinant of the amount of proteinuria or the deterioration of creatinine clearance (Ccr), respectively. Inversely, the deterioration of Ccr was the most important predictor of SM22α expression.
Conclusion: SM22α expression in podocytes and interstitial cells represented the severity of proteinuria and the deterioration of renal function. SM22α expression in renal tissues might be a hallmark of kidney diseases.