Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts
Rev. Assoc. Med. Bras. (1992, Impr.)
; Rev. Assoc. Med. Bras. (1992, Impr.);68(2): 159-164, Feb. 2022. tab, graf
Article
em En
| LILACS
| ID: biblio-1365364
Biblioteca responsável:
BR1.1
ABSTRACT
SUMMARY OBJECTIVE:
The objective of this study was to explore the molecular mechanism underlying the occurrence of benign bile duct stricture and the target of low-dose paclitaxel in the prevention of benign bile duct stricture.METHODS:
Under the stimulation of transforming growth factor beta 1, the expression of collagen type I and connective tissue growth factor were detected on isolated primary fibroblasts. The phosphorylation levels of JNK and Smad2L were detected using Western blot. The effect of low-dose paclitaxel on the transforming growth factor beta 1-induced inhibition of type I collagen and connective tissue growth factor expression and JNK and Smad2L phosphorylation was also observed.RESULTS:
Transforming growth factor beta 1 induced the secretion of type I collagen and connective tissue growth factor as well as JNK phosphorylation in biliary fibroblasts. The JNK inhibitor or siRNA-Smad2 inhibited the transforming growth factor beta 1-induced secretion of type I collagen and connective tissue growth factor. Low-dose paclitaxel inhibited the expression of type I collagen induced by transforming growth factor beta 1 and may inhibit the secretion of collagen in biliary fibroblasts.CONCLUSION:
The activation of JNK/Smad2L induced by transforming growth factor beta 1 is involved in the occurrence of benign bile duct stricture that is mediated by the overexpression of type I collagen and connective tissue growth factor, and low-dose paclitaxel may inhibit the phosphorylation of JNK/Smad2L.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
Assunto principal:
Paclitaxel
Limite:
Humans
Idioma:
En
Revista:
Rev. Assoc. Med. Bras. (1992, Impr.)
Assunto da revista:
EducaÆo em Sa£de
/
GestÆo do Conhecimento para a Pesquisa em Sa£de
/
MEDICINA
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China
País de publicação:
Brasil