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Apoptosis and myofibroblast expression in human glomerular disease: a possible link with transforming growth
Dimitrios S Goumenos1, Athanassios C Tsamandas, A Meguid El Nahas
1Department of Internal Medicine-Nephrology, University Hospital of Patras, GR-26500 Patras, Greece. dgoumenos@med.upatras.gr
Background/Aims:
The pathophysiological pathways involved in the pathogenesis and evolution of renal fibrosis, have not been fully elucidated. Transforming growth factor-beta(1) (TGF-beta(1)) is involved in the development of renal scarring. Apoptosis is responsible for intrinsic cell deletion observed in end-stage kidney disease. Myofibroblasts are involved in the development of renal fibrosis. This study investigates whether there is a potential relationship between apoptosis, myofibroblast infiltration and TGF-beta(1) expression in the kidney of patients with glomerulonephritis (GN).
Methods:
Forty patients with various types of GN were included in the study. Myofibroblasts and TGF-beta(1) positive cells were detected in kidney biopsies by immunohistochemistry, while apoptotic cells were detected by the in situ end labelling of fragmented DNA.
Results:
Myofibroblasts were identified in the glomeruli of some patients with severe mesangioproliferative GN and glomerulosclerosis but a more intensive myofibroblast expression was found in the renal interstitium. TGF-beta(1) was expressed in the cytoplasm of tubular epithelial cells, in the renal interstitium and in the glomeruli of patients with GN. Apoptotic cells were mainly detected in the tubules and interstitium and were present in areas with intense myofibroblast infiltration. Positive correlations were observed between the intensity of myofibroblast expression in the interstitium and apoptosis in the tubulointerstitial area (r = 0.521, p < 0.01) as well as TGF-beta(1) expression (r = 0.462, p < 0.05) and degree of renal impairment (r = 0.430, p < 0.05).
Conclusions:
These observations suggest that myofibroblast infiltration and apoptosis along with TGF-beta(1) expression are associated with the development of interstitial fibrosis in patients with glomerular disease.
Insights
Myofibroblast infiltration, apoptosis, and transforming growth factor-beta(1) (TGF-beta(1)) are linked to interstitial fibrosis in kidney disease. These factors correlate with disease severity and renal impairment in patients with glomerulonephritis.
Area of Science:
- Nephrology
- Pathology
- Cell Biology
Background:
- Renal fibrosis pathogenesis is not fully understood.
- Transforming growth factor-beta(1) (TGF-beta(1)) and apoptosis are implicated in kidney scarring and end-stage kidney disease.
- Myofibroblasts contribute to renal fibrosis development.
Purpose of the Study:
- To investigate the relationship between apoptosis, myofibroblast infiltration, and TGF-beta(1) expression in glomerulonephritis (GN).
Main Methods:
- Immunohistochemistry was used to detect myofibroblasts and TGF-beta(1) in kidney biopsies from 40 GN patients.
- In situ end labeling detected apoptotic cells in kidney tissues.
Main Results:
- Myofibroblast expression was prominent in the renal interstitium.
- TGF-beta(1) was detected in tubular epithelial cells, interstitium, and glomeruli.
- Apoptotic cells were found in tubules and interstitium, correlating with myofibroblast infiltration, TGF-beta(1) expression, and renal impairment.
Conclusions:
- Myofibroblast infiltration, apoptosis, and TGF-beta(1) expression are associated with interstitial fibrosis in glomerular diseases.
- These findings highlight key cellular and molecular players in the progression of kidney fibrosis.