ArticleDigestive diseases and sciences1999
Molecular basis of altered contractility in experimental colitis: expression of L-type calcium channel.
Article in Digestive diseases and sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- The effect of sphingosine-1-phosphate on colonic smooth muscle contractility: Modulation by TNBS-induced colitis.PloS one · 2017Article
- Mechanism of regulation of Na-H exchanger in inflammatory bowel disease: role of TLR-4 signaling mechanism.Digestive diseases and sciences · 2011Article
- Mechanism of reduced colonic contractility in experimental colitis: role of sarcoplasmic reticulum pump isoform-2.Molecular and cellular biochemistry · 2007Article
- Effect of pinaverium bromide on stress-induced colonic smooth muscle contractility disorder in rats.World journal of gastroenterology · 2003Article
- Selective suppression of renal Na+/H+ exchanger isoform-3 by prolonged stimulation of rats with adrenocorticotropic hormone.Endocrine · 2001Article
- Morphological and functional alterations of the myenteric plexus in rats with TNBS-induced colitis.Neurochemical research · 2001Article
- Expression and sub cellular localization of the sodium hydrogen exchanger isoform-1 in rat tissues: a possible functional relevance.Molecular and cellular biochemistry · 2001Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colitis in experimental animals or idiopathic inflammatory bowel disease, such as ulcerative colitis or Crohn's disease in humans, is associated with reduced muscle contraction. This is predicted to be due to disturbance of Ca2+ homeostasis in the inflamed muscle cell. However, the underlying molecular mechanism remains to be elucidated. Since the catalytic alpha-1 subunit of the L-type Ca2+ channel regulates Ca2+ influx, levels of the alpha-1 mRNA and protein were examined. Colitis induced by intrarectal administration of trinitrobenzenesulfonic acid was monitored by measuring the myeloperoxidase activity and histology. The levels of mRNA and protein were estimated using RT-PCR and immunoblotting. Myeloperoxidase activity increased in the inflamed colon, and the lamina propria and muscle layers showed infiltration of inflammatory cells and loss of crypts. Two alternatively spliced alpha-1 mRNA isoforms were detected in the colonic muscle. The ratio of unspliced to spliced mRNA isoforms remained unaltered in inflamed muscle. In contrast, the level of corresponding protein isozymes decreased in the colitic animals. Thus colitis-induced reduction in the alpha-1 protein may account for the reduced colonic contractility seen in colitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.