Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts
Rev. Assoc. Med. Bras. (1992)
;
68(2): 159-164, Feb. 2022. tab, graf
Artículo
en Inglés
| LILACS
| ID: biblio-1365364
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.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
Paclitaxel
Límite:
Humanos
Idioma:
Inglés
Revista:
Rev. Assoc. Med. Bras. (1992)
Año:
2022
Tipo del documento:
Artículo
País de afiliación:
China
Institución/País de afiliación:
Hospital of Xian Jiaotong University/CN
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