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Open AccessArticle

Deletion of SOCS2 Reduces Post-Colitis Fibrosis via Alteration of the TGFβ Pathway

1
Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, P.O box 35, P.C 123, Muscat 113, Oman
2
Department of Physiology, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 113, Oman
3
Department of Pathology, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 113, Oman
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(9), 3073; https://doi.org/10.3390/ijms21093073
Received: 16 March 2020 / Revised: 31 March 2020 / Accepted: 5 April 2020 / Published: 27 April 2020
(This article belongs to the Section Biochemistry)
Inflammatory bowel disease (IBD) is an immunologically mediated chronic intestinal disorder. Growth hormone (GH) administration enhances mucosal repair and decreases intestinal fibrosis in patients with IBD. In the present study, we investigated the effect of cellular sensitivity to GH via suppressor of cytokine signaling 2 (SOCS2) deletion on colitis and recovery. To induce colitis, wild type and SOCS2 knockout (SOCS2−/−) mice were treated with 3% dextran sodium sulphate (DSS), followed by a recovery period. SOCS2−/− mice showed higher disease activity during colitis with increased mRNA expression of the pro-inflammatory cytokines nitric oxide synthase 2 (NOS2) and interleukin 1 β (IL1-β). At recovery time point, SOCS2−/− showed better recovery with less fibrosis measured by levels of α-SMA and collagen deposition. Protein and mRNA expressions of transforming growth factor beta β1 (TGF-β1) receptors were significantly lower in SOCS2−/− mice compared to wild-type littermates. Using an in vivo bromodeoxyuridine (BrdU) proliferation assay, SOCS2−/− mice showed higher intestinal epithelial proliferation compared to wild-type mice. Our results demonstrated that deletion of the SOCS2 protein results in higher growth hormone sensitivity associated with higher pro-inflammatory signaling; however, it resulted in less tissue damage with less fibrotic lesions and higher epithelial proliferation, which are markers of GH-protective effects in IBD. This suggests a pleiotropic effect of SOCS2 and multiple cellular targets. Further study is required to study role of SOCS2 in regulation of TGFβ-mothers against the decapentaplegic homolog (Smad) pathway. View Full-Text
Keywords: inflammatory bowel disease; colitis; growth hormone; suppressor of cytokine signaling protein; fibrosis inflammatory bowel disease; colitis; growth hormone; suppressor of cytokine signaling protein; fibrosis
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Al-Araimi, A.; Al Kharusi, A.; Bani Oraba, A.; Al-Maney, M.M.; Al Sinawi, S.; Al-Haddabi, I.; Zadjali, F. Deletion of SOCS2 Reduces Post-Colitis Fibrosis via Alteration of the TGFβ Pathway. Int. J. Mol. Sci. 2020, 21, 3073.

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