| Expression of transforming growth factor-in human glonierular diseasesEvidence indicates a key role for transforming growth factor-β1 (TGF-β1) in the accumulation of pathologic extracellular matrix in experimental glomerular injury. The aim of this study was to elucidate the expression of TGF-β1 TGF B R 1 and 11 and their role is human glomerulonephritis.TGF-β1 is a multifunctional regulator of cell growth and functions. It regulates many aspects of cellular function. Including proliferation , adhesion, migration and extracellular matrix for mation. It is known that in diseased glomeruli, TGF-β facilitates matrix accumulation in at least three ways by inducing, (1)increased synthesis of matrix proteins, (2)increased synthesis of integrins involved in matrix assembly at the cell surface, and (3)increased synthesis and matrix deposition of protease inhibitors, there by decreasing matrix degradation.MethodsKidney Samples: Needle biopsy specimens of human kidney tissue remaining after diagnostic evaluation were obtained from China Medical University. The patients were diagnosed prior to our study according to standard criteria. Biopsy tissue from 41 case patients included the following distribution of disease: MSPGN 22 cases; MPGN 6 cases; FGS 9 cases; MN 4 cases; three normal kidney Samples were used as control tissues.Immunohistochemistry: Renal biopsies were stained by immunohistological examination. Glomerular expression of TGF-β, and TGF-β R J and II was graded semiquantitatively and reflected changes in and intensity of staining in whole glomeruli: O=background staining; (+)=mildi; (++)=moderate increase in staining; (+++)=marked increase in staining.Statistical analysis: Differences between groups were analyzed by theRidit's analysis and x2-Test; Correlations between the staining intensity of the TGF-β , TGF B R I and II and that of FN and so on were analyzed using Spearman's analysis and Fisher's discrimination.ResultsIn normal kidneys, slight immunoreactivity for the TGF B ,,, TGF P R I and 11 were observed in glomemli and in tubulointerstitial.ln disorder's with abnomial glomerular and tubulointerstitial matrix accumulation, significant increases in the immunoreactivity of the TGF-β , TGF B R I and II were noted in glomeruli and tubulointerstitium (P<0.05), Of MPGN staining intensity was more than others in glomeruli. The tubulointerstitial immunostaining of the TGF- B P TGF P R I and II was similar to that of disorders with abnormal glomerular and tubulointerstitial matrix accumulation including MsPGN, FGS, MN.Immunoreactivty for all was both intracellular and associated with the matrix in the glomeruli and the tubulointerstitium. Differuse and strong intraglomerular staining of the TGF-β n TGF B R 1 and II was found in diffuse proliferative nephritis, crescentic glomerulonephritis, while segmental intraglomerular staining was observed in MsPGN > focal and segmental glomerulsclerosis and focal proliferative nephritis. The Bowan's capsules, crescents, and the tubulointerstitial lesions with matrix deposition showed remarkably strong immuno staining of the TGF-β , > TGF B R 1 and II. The interstitial arteries with intimal thinkening were also positively stained.Correlation between TGF-β ( and TGF B R I > II . To determine whether expression of each receptor was equally related to the TGF-β , in human glomerular diseases. Spearman's analysis was performed. The result indicate that the levels of glomerular and tubulointerstitial deposition of TGF- P type 1 receptor and TGF-β type II receptor were significantly correlated.Deposition of FN, FRA, a 2-Pl, PLG. In normal kidneys, trace deposits were observed in glomeruli and the interstitium. In MsPGN focal and segmental glomerulosclerosis, crescentic glomerulonephritis,membranous mephropathy. Significantly increased deposition was noted in glomeruli showing mesangial matrix accumulation, in the crescents, and in the periglomerular and tubulointerstitial lesion and increased interstitial matrix deposi... |
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