High nitric oxide synthase activity in endothelial cells in ulcerative colitis

Iwashita, Etsuro; Miyahara, Toru; Hino, Kunihiko; Tokunaga, Tetsuji; Wakisaka, Hitoshi; Sawazaki, Yoshio

doi:10.1007/bf02347578

Cited by 22 publications

(11 citation statements)

References 15 publications

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“…Elevated levels of eNOS have been found both in colonic tissue from DSSinduced colitis in mice (4) and in mesenteric endothelial cells from patients with ulcerative colitis (16).…”

Section: Discussionmentioning

confidence: 99%

eNOS involved in colitis-induced mucosal blood flow increase

Petersson¹,

Schreiber²,

Steege³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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The role of NO in inflammatory bowel disease is controversial. Studies indicate that endothelial nitric oxide synthase (eNOS) might be involved in protecting the mucosa against colonic inflammation. The aim of this study was to investigate the involvement of nitric oxide (NO) in regulating colonic mucosal blood flow in two different colitis models in rats. In anesthetized control and colitic rats, the distal colon was exteriorized and the mucosa visualized. Blood flow (laser-Doppler flowmetry) and arterial blood pressure were continuously monitored throughout the experiments, and vascular resistance was calculated. Trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) was used to induce colitis. All groups were given the NOS inhibitor N(omega)-nitro-l-arginine (l-NNA) or the inducible NOS (iNOS) inhibitor l-N(6)-(1-iminoethyl)-lysine (l-NIL). iNOS, eNOS, and neuronal NOS (nNOS) mRNA in colonic samples were investigated with real-time RT-PCR. Before NOS inhibition, colonic mucosal blood flow, expressed as perfusion units, was higher in both colitis models compared with the controls. The blood flow was reduced in the TNBS- and DSS-treated rats during l-NNA administration but was not altered in the control group. Vascular resistance increased more in the TNBS- and DSS-treated rats than in the control rats, indicating a higher level of vasodilating NO in the colitis models. l-NIL did not alter blood pressure or blood flow in any of the groups. iNOS and eNOS mRNA increased in both colitis models, whereas nNOS remained at the control level. TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity.

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“…Elevated levels of eNOS have been found both in colonic tissue from DSSinduced colitis in mice (4) and in mesenteric endothelial cells from patients with ulcerative colitis (16).…”

Section: Discussionmentioning

confidence: 99%

eNOS involved in colitis-induced mucosal blood flow increase

Petersson¹,

Schreiber²,

Steege³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…38 NO is an effector molecule for intestinal epithelia injury in humans and mice. [39][40][41][42] A combination of TNF-a and IFN-c is most potent for stimulation of inducible NO synthase induction. 43 44 Thus impaired production of IL-12p40, TNF-a, and IFN-c in LP cells of IL-15 KO mice may be mainly due to amelioration of DSS induced acute colitis in IL-15 KO mice.…”

Section: Discussionmentioning

confidence: 99%

Role of interleukin 15 in colitis induced by dextran sulphate sodium in mice

Yoshihara

Yajima

Kubo³

et al. 2006

Gut

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Background and aims: Interleukin (IL)-15 is a member of the IL-2 family, stimulating dendritic cells, natural killer (NK) cells, NK T cells and memory CD8 + T cells. IL-15 levels were elevated in the intestinal mucosa of inflammatory bowel diseases. Here we investigated the involvement of IL-15 in the pathogenesis of acute and chronic dextran sulphate sodium (DSS) induced colitis. Methods: IL-15 knockout (KO) mice and control C57BL/6 mice were used to induce colitis with DSS in their drinking water. Survival rate, clinical activity of diseases, extent of tissue damage, leucocyte population, and cytokine production of lamina propria (LP) cells of the large intestines were assessed.

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“…This is indicative of a reaction between NO and superoxide. In active ulcerative colitis, increased NOS activity has also been found in microvascular endothelial cells from the colonic mesentery [108].…”

Section: Nitric Oxide In Chronic Gut Inflammationmentioning

confidence: 98%

Role of Nitric Oxide in Gastrointestinal Inflammatory and Ulcerative Diseases: Perspective for Drugs Development

Barrachina¹,

Panés²,

Esplugues³

2001

CPD

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Nitric oxide is a ubiquitous molecule involved in a variety of biological processes. The specific action of NO depends on its enzymatic sources namely neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS) and all three isoforms have been localized in the gastrointestinal tract. Constitutive synthesis of NO by nNOS or eNOS isoforms is involved in the maintaining of the gastrointestinal mucosal integrity through modulation of gastric mucosal blood flow, epithelial secretion and barrier function. However, large amounts of NO synthesized from the inducible isoform have been implicated in tissue injury in the gut during inflammatory reactions. In this review we provide an overview of the dual role of nitric oxide in modulating gastrointestinal mucosal defense and injury. In addition, we highlight the therapeutic potential of NO modulation.

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High nitric oxide synthase activity in endothelial cells in ulcerative colitis

Cited by 22 publications

References 15 publications

eNOS involved in colitis-induced mucosal blood flow increase

eNOS involved in colitis-induced mucosal blood flow increase

Role of interleukin 15 in colitis induced by dextran sulphate sodium in mice

Role of Nitric Oxide in Gastrointestinal Inflammatory and Ulcerative Diseases: Perspective for Drugs Development

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