ArticleNeurogastroenterology and motility2010
CaM kinase II in colonic smooth muscle contributes to dysmotility in murine DSS-colitis.
Article in Neurogastroenterology and motility, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- TGF-β1-induced phospholamban expression alters esophageal smooth muscle cell contraction in patients with eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2014Trial
- Jianpi Qingchang decoction regulates intestinal motility of dextran sulfate sodium-induced colitis through reducing autophagy of interstitial cells of Cajal.World journal of gastroenterology · 2017Article
- The Involvement of Ca(2+) Signal Pathways in Distal Colonic Myocytes in a Rat Model of Dextran Sulfate Sodium-induced Colitis.Chinese medical journal · 2016Article
- Tra2β protein is required for tissue-specific splicing of a smooth muscle myosin phosphatase targeting subunit alternative exon.The Journal of biological chemistry · 2012Article
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- Regulation of basal LC20 phosphorylation by MYPT1 and CPI-17 in murine gastric antrum, gastric fundus, and proximal colon smooth muscles.Neurogastroenterology and motility · 2011Article
- Regulation of gastrointestinal motility by Ca2+/calmodulin-stimulated protein kinase II.Archives of biochemistry and biophysics · 2011Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAltered calcium mobilization has been implicated in the development of colonic dysmotility in inflammatory bowel disease. The aim of this study was to investigate the mechanisms by which disrupted intracellular Ca(2+) signalling contributes to the impaired contractility of colon circular smooth muscles.
methodsAcute colitis was induced in C57Bl/6 mice with dextran sulphate sodium (DSS) in the drinking water for 5 days. KEY
resultsSpontaneous and acetylcholine-evoked contractions, caffeine-evoked hyperpolarization, and SERCA2 and phospholamban expression were reduced compared with controls. Tetrodotoxin did not restore control levels of contractile activity. The amplitudes, but not the frequency, of intracellular Ca(2+) waves were increased compared with controls. Caffeine abolished intracellular Ca(2+) waves in control smooth muscle cells, but not in smooth muscle cells from DSS-treated mice. CaM kinase II activity and cytosolic levels of HDAC4 were increased, and I kappaB alpha levels were decreased in distal colon smooth muscles from DSS-treated mice. CONCLUSIONS & INFERENCES: These results suggest that disruptions in intracellular Ca(2+) mobilization due to down-regulation of SERCA2 and phospholamban expression lead to increased CaM kinase II activity and cytosolic HDAC4 that may contribute to the dysmotility of colonic smooth muscles in colitis by enhancing NF-kappaB activity.
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