ISSN:
1437-7799
Keywords:
Key wordsα-Smooth muscle actin
;
Myosin heavy chain
;
Caldesmon
;
Tropomyosin
;
Mesangial cell
;
Interstitial cell
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Background. Phenotypic changes in glomerular mesangial cells and interstitial cells are considered to be closely associated with the progression of glomerulosclerosis and renal fibrosis in IgA nephropathy. To further evaluate the relevance of phenotypic changes, we examined the expression of four different contractile proteins as markers of the phenotypic changes. Methods. The expression of nonmuscle myosin heavy chain isoform (SMemb), α-smooth muscle actin (α-SMA), caldesmon (CaD), and tropomyosin (TM) was evaluated by indirect immunofluorescent studies in renal biopsy specimens from 21 patients with IgA nephropathy. The relationships with the histological parameters and clinical parameters were analyzed. Results. Pronounced expression (score of 2 or more) of contractile proteins was observed in the majority of the patients (57%–90%) compared with controls. There was no significant relationship between the glomerular expression score of any contractile protein and the proliferation index or sclerotic index. Daily urinary protein excretion in the group expressing low levels of caldesmon in the glomerulus was significantly lower than that in the group expressing high levels (P 〈 0.05). There were significant correlations among the glomerular expressions of these contractile proteins, except for TM (P 〈 0.05). All contractile proteins were expressed in tubulointerstitial lesions, and only SMemb expression was detected in tubular epithelial cells. The interstitial scores of all contractile proteins increased in parallel with the degree of tubulointerstitial lesion (P 〈 0.05). Conclusions. Contractile proteins appeared to be coordinately expressed in the glomerulus and the interstitium in IgA nephropathy, which may reflect the mechanical stress involved with glomerulonephritis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s101570050048
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