Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Revista da Associação Médica Brasileira (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0104-42302022000200159 |
Resumo: | 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. |
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Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblastsBile ductFibroblastsJNKSmadPaclitaxelSUMMARY 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.Associação Médica Brasileira2022-02-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0104-42302022000200159Revista da Associação Médica Brasileira v.68 n.2 2022reponame:Revista da Associação Médica Brasileira (Online)instname:Associação Médica Brasileira (AMB)instacron:AMB10.1590/1806-9282.20210777info:eu-repo/semantics/openAccessLu,JiameiYu,LiangShi,Jianhuaeng2022-09-01T00:00:00Zoai:scielo:S0104-42302022000200159Revistahttps://ramb.amb.org.br/ultimas-edicoes/#https://old.scielo.br/oai/scielo-oai.php||ramb@amb.org.br1806-92820104-4230opendoar:2022-09-01T00:00Revista da Associação Médica Brasileira (Online) - Associação Médica Brasileira (AMB)false |
dc.title.none.fl_str_mv |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
title |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
spellingShingle |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts Lu,Jiamei Bile duct Fibroblasts JNK Smad Paclitaxel |
title_short |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
title_full |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
title_fullStr |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
title_full_unstemmed |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
title_sort |
Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts |
author |
Lu,Jiamei |
author_facet |
Lu,Jiamei Yu,Liang Shi,Jianhua |
author_role |
author |
author2 |
Yu,Liang Shi,Jianhua |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Lu,Jiamei Yu,Liang Shi,Jianhua |
dc.subject.por.fl_str_mv |
Bile duct Fibroblasts JNK Smad Paclitaxel |
topic |
Bile duct Fibroblasts JNK Smad Paclitaxel |
description |
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. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-02-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0104-42302022000200159 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0104-42302022000200159 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/1806-9282.20210777 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Associação Médica Brasileira |
publisher.none.fl_str_mv |
Associação Médica Brasileira |
dc.source.none.fl_str_mv |
Revista da Associação Médica Brasileira v.68 n.2 2022 reponame:Revista da Associação Médica Brasileira (Online) instname:Associação Médica Brasileira (AMB) instacron:AMB |
instname_str |
Associação Médica Brasileira (AMB) |
instacron_str |
AMB |
institution |
AMB |
reponame_str |
Revista da Associação Médica Brasileira (Online) |
collection |
Revista da Associação Médica Brasileira (Online) |
repository.name.fl_str_mv |
Revista da Associação Médica Brasileira (Online) - Associação Médica Brasileira (AMB) |
repository.mail.fl_str_mv |
||ramb@amb.org.br |
_version_ |
1754212837322915840 |