Excessive nitric oxide (NO) generated by hepatic cells in response to lipopolysaccharide (LPS) and inflammatory substances (e.g., platelet-activating factor [PAF]) is a key contributor to the pathophysiological outcomes observed in the liver during sepsis. In rats subjected to liver-focused endotoxe
Functional activity and expression of inducible nitric oxide synthase (iNOS) in muscle of the isolated distal colon of mdx mice
โ Scribed by Maria Giuliana Vannucchi; Letizia Corsani; Gian Battista Azzena; Maria Simonetta Faussone-Pellegrini; Rino Mancinelli
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 339 KB
- Volume
- 29
- Category
- Article
- ISSN
- 0148-639X
No coin nor oath required. For personal study only.
โฆ Synopsis
Abstract
The inducible isoform of nitric oxide (NO) synthase (iNOS), expressed in endothelium, epithelium, and inflammatory cells, produces a large amount of NO. Previous studies on mouse intestine indicate that a muscular iNOS may have a role in the storage of intraluminal content. In this study we investigated the presence and function of iNOS in the colonic smooth muscle cells of 2โ and 12โmonthโold dystrophic (mdx) mice. By using an in vitro isovolumic technique, and immunohistochemical and Western blot analysis, we demonstrated that iNOS is expressed and active in the smooth muscle cells of normal mouse and defective in young adult (2โmonthโold) mdx mice. Therefore, an altered activity of the muscle iNOS might explain the motility disorders observed in the colon of mdx mice and, from a clinical point of view, the impairment of intestinal function in dystrophic patients. Muscle Nerve 29: 795โ803, 2004
๐ SIMILAR VOLUMES
## Abstract Since NO production by NOSโ2 made by astrocytes activated by proinflammatory cytokines contributes to the killing of neurons in variously damaged human brains, knowing the mechanisms responsible for NOSโ2 expression should contribute to developing effective therapeutics. The expression