Interaction between sphingosine ...
Document type :
Article dans une revue scientifique
DOI :
PMID :
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Title :
Interaction between sphingosine kinase/sphingosine 1 phosphate and transforming growth factor-β/Smads pathways in experimental intestinal fibrosis. An in vivo immunohistochemical study.
Author(s) :
Sferra, Roberta [Auteur]
Pompili, Simona [Auteur]
Ventura, Luca [Auteur]
Dubuquoy, Caroline [Auteur]
Speca, Silvia [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gaudio, Eugenio [Auteur]
Latella, Giovanni [Auteur]
Vetuschi, Antonella [Auteur]
Pompili, Simona [Auteur]
Ventura, Luca [Auteur]
Dubuquoy, Caroline [Auteur]
Speca, Silvia [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gaudio, Eugenio [Auteur]
Latella, Giovanni [Auteur]
Vetuschi, Antonella [Auteur]
Journal title :
European Journal of Histochemistry
Abbreviated title :
Eur J Histochem
Volume number :
62
Publication date :
2018-07-24
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
A concomitant action of multiple profibrotic mediators appears crucial in the development and progression of fibrosis. Sphingosine kinase/sphingosine 1 phosphate and transforming growth factor-beta/Smads pathways are ...
Show more >A concomitant action of multiple profibrotic mediators appears crucial in the development and progression of fibrosis. Sphingosine kinase/sphingosine 1 phosphate and transforming growth factor-beta/Smads pathways are both involved in pathogenesis of fibrosis in several organs by controlling differentiation of fibroblasts to myofibroblasts and the epithelial to-mesenchymal transition. However, their direct involvement in chronic colitis-associated fibrosis it is not yet known. In this study we evaluated the immunohistochemical expression of some proteins implicated in sphingosine kinase/sphingosine 1 phosphate and transforming growth factor-beta/Smads pathways in Dextrane Sodium Sulphate (DSS)-induced colorectal fibrosis in mice. Compared to control mice, DSS-induced chronic colitis mice developed a marked intestinal fibrosis associated with a concomitant overexpression of TGF-beta, p-Smad3, alpha-SMA, collagen I-III, SPHK1, RhoA, PI3K, Akt, p-Akt, p-mTOR. This study highlights the relationship between the two pathways and the possible role of SPHK1 in the intestinal fibrosis. These results, if confirmed by in vitro studies, may have important clinical implications in the development of new therapeutical approaches in inflammatory bowel disease.Show less >
Show more >A concomitant action of multiple profibrotic mediators appears crucial in the development and progression of fibrosis. Sphingosine kinase/sphingosine 1 phosphate and transforming growth factor-beta/Smads pathways are both involved in pathogenesis of fibrosis in several organs by controlling differentiation of fibroblasts to myofibroblasts and the epithelial to-mesenchymal transition. However, their direct involvement in chronic colitis-associated fibrosis it is not yet known. In this study we evaluated the immunohistochemical expression of some proteins implicated in sphingosine kinase/sphingosine 1 phosphate and transforming growth factor-beta/Smads pathways in Dextrane Sodium Sulphate (DSS)-induced colorectal fibrosis in mice. Compared to control mice, DSS-induced chronic colitis mice developed a marked intestinal fibrosis associated with a concomitant overexpression of TGF-beta, p-Smad3, alpha-SMA, collagen I-III, SPHK1, RhoA, PI3K, Akt, p-Akt, p-mTOR. This study highlights the relationship between the two pathways and the possible role of SPHK1 in the intestinal fibrosis. These results, if confirmed by in vitro studies, may have important clinical implications in the development of new therapeutical approaches in inflammatory bowel disease.Show less >
Language :
Anglais
Audience :
Internationale
Popular science :
Non
Administrative institution(s) :
Inserm
Université de Lille
CHU Lille
Université de Lille
CHU Lille
Research team(s) :
Inflammatory digestive disease : pathophysiology and therapeutic targets developement
Submission date :
2019-03-01T14:08:02Z
2024-03-05T12:03:55Z
2024-03-05T12:03:55Z
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