Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis

Shi, Xuan; Winston, John H.; Sarna, Sushil K.

doi:10.1152/ajpgi.00358.2010

Cited by 76 publications

(98 citation statements)

References 50 publications

(62 reference statements)

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“…Sato et al (48), however, reported hypocontractility of mouse colonic circular smooth muscle obtained from DSS-treated colon that was mediated by a decrease in CPI-17 expression. Their findings are similar to those previously by others and us in circular smooth muscle exposed to IL-1␤ or obtained from TNBS-treated colon (16,43,52). Shi and co-workers (52) have reported that decrease in circular muscle contraction obtained from DSS-treated rat colon was due to suppression of G␣ q protein, whereas in TNBS-treated rat colon was due to suppression of ␣ 1c 1b subunit of Ca v 1.2 b channels, G␣ q and CPI-17.…”

Section: Discussionsupporting

confidence: 92%

“…Shi and co-workers (52) have reported that decrease in circular muscle contraction obtained from DSS-treated rat colon was due to suppression of G␣ q protein, whereas in TNBS-treated rat colon was due to suppression of ␣ 1c 1b subunit of Ca v 1.2 b channels, G␣ q and CPI-17. Several cytokines and chemokines including IL-1␤, TNF-␣, IL-6, monocyte chemoattractant protein (MCP-1), and IL-8 are shown to be increased in mucosa/submucosa and muscularis externa from day 1 to day 7 of TNBS inflammation (52). The expression of cytokine profile in longitudinal muscle vs. circular muscle is not known.…”

Section: Discussionmentioning

confidence: 99%

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Jun kinase-induced overexpression of leukemia-associated Rho GEF (LARG) mediates sustained hypercontraction of longitudinal smooth muscle in inflammation

Al‐Shboul

Nalli

Kumar

et al. 2014

American Journal of Physiology-Cell Physiology

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Al-Shboul O, Nalli AD, Kumar DP, Zhou R, Mahavadi S, Kuemmerle JF, Grider JR, Murthy KS. Jun kinase-induced overexpression of leukemia-associated Rho GEF (LARG) mediates sustained hypercontraction of longitudinal smooth muscle in inflammation. Am J Physiol Cell Physiol 306: C1129 -C1141, 2014. First published April 16, 2014; doi:10.1152/ajpcell.00021.2014.-The signaling pathways mediating sustained contraction of mouse colonic longitudinal smooth muscle and the mechanisms involved in hypercontractility of this muscle layer in response to cytokines and TNBS-induced colitis have not been fully explored. In control longitudinal smooth muscle cells, ACh acting via m3 receptors activated sequentially G␣12, RhoGEF (LARG), and the RhoA/Rho kinase pathway. There was abundant expression of MYPT1, minimal expression of CPI-17, and a notable absence of a PKC/CPI-17 pathway. LARG expression was increased in longitudinal muscle cells isolated from muscle strips cultured for 24 h with IL-1␤ or TNF-␣ or obtained from the colon of TNBS-treated mice. The increase in LARG expression was accompanied by a significant increase in ACh-stimulated Rho kinase and ZIP kinase activities, and sustained muscle contraction. The increase in LARG expression, Rho kinase and ZIP kinase activities, and sustained muscle contraction was abolished in cells pretreated with the Jun kinase inhibitor, SP600125. Expression of the MLCP activator, telokin, and MLCP activity were also decreased in longitudinal muscle cells from TNBS-treated mice or from strips treated with IL-1␤ or TNF-␣. In contrast, previous studies had shown that sustained contraction in circular smooth muscle is mediated by sequential activation of G␣13, p115RhoGEF, and dual RhoA-dependent pathways involving phosphorylation of MYPT1 and CPI-17. In colonic circular smooth muscle cells isolated from TNBS-treated mice or from strips treated with IL-1␤ or TNF-␣, CPI-17 expression and sustained muscle contraction were decreased. The disparate changes in the two muscle layers contribute to intestinal dysmotility during inflammation.colon; contraction; cytokines; signaling GASTROINTESTINAL smooth muscle exhibits regional variations in expression of structural, contractile, and signaling proteins that can influence its response to a variety of regulatory agents (e.g., acetylcholine, biogenic amines, neuropeptides, pyrimidines/purines; lipids, and cytokines) (3,12,27,37,57). Functional differences are evident between muscle layers (e.g., circular vs. longitudinal muscle of the intestine) or within the same layer (proximal tonic vs. distal rhythmic circular muscle of the stomach) (10,19,31,35,38,58,59). In all types of smooth muscle, an essential requirement for contraction is phosphorylation of the 20-kDa regulatory light chain (MLC) of myosin II (MLC 20 ), which in turn is regulated by the balance between Ca 2ϩ -dependent or -independent MLC kinase (MLCK) activity and MLC phosphatase (MLCP) activity (8,13,25,37,55).In both circular and longitudinal intestinal smooth muscle, contraction in respo...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Jun kinase-induced overexpression of leukemia-associated Rho GEF (LARG) mediates sustained hypercontraction of longitudinal smooth muscle in inflammation

Al‐Shboul

Nalli

Kumar

et al. 2014

American Journal of Physiology-Cell Physiology

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“…They allow a detailed examination of the pathological process from acute to chronic phase, providing an insight into the immunological disturbances behind the pathogenesis of IBD (Hibi et al, 2008;Mizoguchi & Mizoguchi, 2010;Shi et al, 2011). In these animal models colitis can be induced by chemical, immunological, microbiological and physical factors (Boirivant et al, 1998;Morris et al, 1989;Okayasu et al, 1990).…”

Section: Bmps and Tgfβ/bmp Signaling Pathway In Inflammatory Bowel DImentioning

confidence: 99%

Bone Morphogenetic Proteins and Signaling Pathway in Inflammatory Bowel Disease

Marić¹,

Wensveen²,

Smoljan³

et al. 2012

Inflammatory Bowel Disease - Advances in Pathogenesis and Management

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“…Intra-colonic administration of trinitrobenzene sulfonic acid (TNBS) is one of standardized methods to produce an experimental model of IBD, which closely mimic the clinical and morphological features of IBD in particular Crohn's disease [17].…”

Section: Introductionmentioning

confidence: 99%

Protective effect of ellagic acid, a natural polyphenolic compound, in a murine model of Crohn's disease

Rosillo

Sánchéz-Hidalgo

Cárdeno

et al. 2011

Biochemical Pharmacology

149

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 of 37A c c e p t e d M a n u s c r i p t

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Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis

Abstract: Shi XZ, Winston JH, Sarna SK. Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis.

Cited by 76 publications

References 50 publications

Jun kinase-induced overexpression of leukemia-associated Rho GEF (LARG) mediates sustained hypercontraction of longitudinal smooth muscle in inflammation

Jun kinase-induced overexpression of leukemia-associated Rho GEF (LARG) mediates sustained hypercontraction of longitudinal smooth muscle in inflammation

Bone Morphogenetic Proteins and Signaling Pathway in Inflammatory Bowel Disease

Protective effect of ellagic acid, a natural polyphenolic compound, in a murine model of Crohn's disease

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