Dextran sodium sulphate (DSS)-induced colitis alters the expression of neurotrophins in smooth muscle cells of rat colon

Title:

Dextran sodium sulphate (DSS)-induced colitis alters the expression of neurotrophins in smooth muscle cells of rat colon

Creator:

Al-Qudah, M., Shammala, D. A., Al-Dwairi, A., Al-Shboul, O., and Mustafa, A. G.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:132b7423-bd20-4417-949f-6741f643d8b6
uuid:132b7423-bd20-4417-949f-6741f643d8b6

Subject:

neurotrophins, gastrointestinal Tract, Gut Smooth Muscle, Inflammation, DSS, and colitis

Type:

article, model:article, and TEXT

Description:

Neurotrophins are present in the gastrointestinal tract where they participate in the survival and growth of enteric neurons, augmentation of enteric circuits, elevation of colonic myoelectrical activity and also in different aspects of colitis. Previous studies largely focused on the role of neural and mucosal neurotrophins in gut inflammation. The expression of neurotrophins in colonic smooth muscle cells (SMCs) and the interactions of this potential source with colitis has not been studied in the gut. The expression of NGF, BDNF, NT-3 and NT-4 in SMCs from longitudinal and circular muscle layers of rat colon from normal and dextran sodium sulphate (DSS)-induced colitis rats was measured by ELISA. NGF, BDNF, NT-3 and NT-4 are differentially expressed in both longitudinal and circular SMCs, where the expressions of BDNF and NT-4 proteins were greater in SMCs from the longitudinal muscle layer than from the circular muscle layer, while NGF protein expression was greater in circular SMCs and NT-3 expression was equal in cells from both muscle layers. Induction of colitis with DSS significantly alters neurotrophins expression pattern in colonic SMCs. NGF levels upregulated in circular SMCs. BDNF level was increased in DSS-induced colitis in longitudinal SMCs. NGF, NT-3 and NT-4 levels were downregulated in longitudinal SMCs of DSS-induced colitis rats' colon. Disturbances of neurotrophins expression in SMCs resulted from colitis might account for the structural and functional changes in inflammatory bowel disease (IBD) such as loss of innervation and characteristic hypercontractility of longitudinal muscle in IBD.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:6

Harvested from:

CDK

Metadata only:

false