TGF-beta Mediated Epithelial-Mesenchymal Transition in Autosomal Dominant Polycystic Kidney Disease
Yonsei Medical Journal
; : 105-111, 2009.
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| ID: wpr-83524
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ABSTRACT
PURPOSE:
Recent studies have showed that epithelial-mesenchymal transition (EMT) is a key process of glomerular and tubulointerstitial pathology in many chronic kidney diseases. However, there are no data of EMT in humane autosomal dominant polycystic kidney disease (ADPKD). PATIENTS ANDMETHODS:
ADPKD kidneys (N = 5) with end stage renal disease (ESRD) and control kidneys (N = 4) were analyzed immnunohistochemically. We evaluated alpha-SMA, E-cadherin, vimentin, TGF-beta1 and Smad 2/3 expression in ADPKD and compared them with those in control kidney. These immunohistochemical findings were quantitatively analyzed by computer-assisted image analyzer and positive tubules (%).RESULTS:
There were severe interstitial fibrosis and proliferation of alpha-SMA+ myofibroblasts in ADPKD. Cystic tubular epithelial cells in ADPKD lost epithelial marker (E-cadherin) and expressed mesenchymal markers (alpha-SMA, vimentin). There were significant increases of alpha-SMA (34.3 +/- 11.7% vs 0.9 +/- 1.5%), vimentin (19.9 +/- 3.9% vs 3.3 +/- 1.4%), TGF-beta1 (5.42 +/- 2.83% vs 0%) and Smad 2/3 (3.4 +/- 1.7% vs 0.7 +/- 0.6%) in ADPKD kidneys compared with control kidneys evidenced by computer-assisted image analyzer. When we analyze the positive tubules (%), the results were the same as computer-assisted image analyzer.CONCLUSION:
Our results showed that the end stage of ADPKD is associated with TGF-beta, Smad 2/3 and markers of EMT. It suggests that TGF-beta mediated EMT has a role in progression of ADPKD.Palavras-chave
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Assunto principal:
Fibrose
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Biomarcadores
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Divisão Celular
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Fator de Crescimento Transformador beta
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Rim Policístico Autossômico Dominante
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Progressão da Doença
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Células Epiteliais
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Glomérulos Renais
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Túbulos Renais
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Mesoderma
Limite:
Aged
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Female
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Humans
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Male
Idioma:
En
Revista:
Yonsei Medical Journal
Ano de publicação:
2009
Tipo de documento:
Article