Quantitative histological analysis of SM22α (transgelin) in an adriamycin-induced focal segmental glomerulosclerosis model.
OBJECTIVE
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.


CONCLUSIONS
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.
Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Xingzhi
X
Wang
Minoru
M
Sakatsume
Yuichi
Y
Sakamaki
Shigeru
S
Inomata
Tadashi
T
Yamamoto
Ichiei
I
Narita
D000818:Animals; D004195:Disease Models, Animal; D004317:Doxorubicin; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D005923:Glomerulosclerosis, Focal Segmental / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D007150:Immunohistochemistry; D007668:Kidney / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism*; D016253:Microscopy, Immunoelectron; D009124:Muscle Proteins / Q000378:metabolism*; D050199:Podocytes / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D051381:Rats; D017208:Rats, Wistar
D008840:Microfilament Proteins; D009124:Muscle Proteins; C051615:transgelin; D004317:Doxorubicin