Irritant-induced cyclooxygenase-2 is involved in the defense mechanism of the gastric mucosa in mice

Miyake, Kazumasa; Tsukui, Taku; Wada, Ken; Tatsuguchi, Atsushi; Futagami, Seiji; Hiratsuka, Tetsuro; Shinoki, Kei; Iizumi, Tadasu; Akamatsu, Tomonori; Sakamoto, Choitsu; Kobayashi, Masafumi

doi:10.1007/s005350200016

Cited by 11 publications

(9 citation statements)

References 30 publications

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“…First, we examined the localization of COX-2-expressing cells in the stomach of ethanol-treated mice to determine the cells expressing COX-2 in vivo. We expected to detect COX-2 protein in ethanol-treated gastric mucosa as shown by Miyake et al (28) and Bhandari et al (2). We were, however, unable to obtain a clear COX-2 signal in the mucosa of our gastric tissue specimens (data not shown).…”

Section: Discussionsupporting

confidence: 53%

“…The stomachs were removed without using the perfusion process, sectioned horizontally, and either fixed in 10% buffered formalin for histochemistry or immediately frozen in liquid nitrogen for the analysis of RNA, protein, and PGE2. The histologic extent of the gastric mucosal injury was evaluated by a pathologist as the percentage of the length of microscopically identified mucosal injury, which comprised hemorrhage and disruption of gastric epithelial cells to the length of the circumference of the gastric corpus, according to the method described by Miyake et al (28).…”

Section: Methodsmentioning

confidence: 99%

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Protective role of adiponectin against ethanol-induced gastric injury in mice

Yamamoto

Watabe

Araki

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Adiponectin is an anti-inflammatory molecule released from adipocytes, and serum adiponectin concentrations are reduced in obesity. We previously reported that gastric erosion occurs in association with obesity and low serum adiponectin levels. In the present study, we examined adiponectin-knockout (APN-KO) mice to elucidate the role of adiponectin in gastric mucosal injury. Gastric injury was induced by oral administration of ethanol in wild-type (WT) and APN-KO mice. Ethanol treatment induced severe gastric injury in APN-KO mice compared with WT mice. In APN-KO mice, increased apoptotic cells and decreased expression of prostaglandin E(2) (PGE(2)) were detected in the injured stomach. We next assessed the effect of adiponectin on the cellular response to ethanol treatment and wound repair in rat gastric mucosal cells (RGM1). Adiponectin induced the expression of PGE(2) and cyclooxygenase 2 (COX-2) in ethanol-treated RGM1 cells. RGM1 cells exhibited efficient wound repair accompanied by increased PGE(2) expression in the presence of adiponectin. Coadministration of adiponectin with celecoxib, a COX-2 inhibitor, inhibited efficient wound repair. These findings indicate that adiponectin has a protective role against ethanol-induced gastric mucosal injury in mice. This effect may be partially mediated by the efficient wound repair of epithelial cells via increased PGE(2) expression.

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Section: Discussionsupporting

confidence: 53%

Section: Methodsmentioning

confidence: 99%

Protective role of adiponectin against ethanol-induced gastric injury in mice

Yamamoto

Watabe

Araki

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…We should be cautious, therefore, in extrapolating these findings to other mouse strains and should consider taking a multistrain approach in mouse prostanoid research. Furthermore, some of the reports on the role of prostaglandins in gastric acid secretion have been published without mention of the mouse strain used (22,23). Our RT-PCR revealed that the strain difference we have characterized pharmacologically is related to lower expression of message for the EP 3 receptor in gastric mucosa from C57BL/6 than from BALB/c mice.…”

Section: Discussionmentioning

confidence: 73%

Host-specific differences in the physiology of acid secretion related to prostaglandins may play a role in gastric inflammation and injury

Padol¹,

Hunt²

2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Padol, Ireneusz T., and Richard H. Hunt. Host-specific differences in the physiology of acid secretion related to prostaglandins may play a role in gastric inflammation and injury. 14 C]aminopyrine accumulation and pylorus ligation, we aimed to study acid secretion in gastric gland preparations from the commonly used strains of BALB/c and C57BL/6 mice. We found that PGE 2 does not inhibit acid secretion in gastric glands from C57BL/6 mice, in contrast to the expected antisecretory effect of PGE 2 observed in BALB/c mice. In BALB/c mice the effect of histamine and carbachol was reduced by PGE 2, whereas in C57BL/6 mice dose-response curves to these secretagogues were not affected. EP 3 receptors are not involved in acid secretion in C57BL/6 mice, as confirmed by significantly lower expression of mRNA for the EP 3 receptor. These contrary findings are important to the interpretation of the antisecretory role of eicosanoids in BALB/c and C57BL/6 mouse strains and the involvement of prostanoids in the etiology of Helicobacter-induced inflammation and NSAID-induced gastropathies. We propose that the lack of antisecretory effect of PGE 2 observed in C57BL/6 mice could reflect the extent of Helicobacter-induced inflammation and status of acid secretion in response to anti-inflammatory drugs.

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“…Although such low taurocholate doses did not provoke severe gastric damage, this taurocholateinduced adaptive cytoprotection lasted for over 5 h; the early phase shown to be mediated mainly by COX-1, and the latter phase by both COX-1 and COX-2 (29). We also found that, COX-2, induced 24 h after pretreatment with a mild irritant, serves as a defense mechanism by minimizing subsequent irritant-induced damage (30). Taking all these studies into consideration, it is now clear that COX-2 expressed in the injured mucosa plays a significant role in the repair process and in the defense mechanism of the stomach.…”

Section: Role Of Cox-2 In the Gastric Mucosamentioning

confidence: 73%

The Role of Cyclooxygenase in Gastric Mucosal Protection

Gudis

Sakamoto

2005

Dig Dis Sci

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COX-1 and COX-2 are two cyclooxygenase enzymes responsible for prostanoid production. COX-2 is expressed in inflammatory cells and fibroblasts of the gastric mucosa, and through the production of various growth factors including hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF), plays a key role in the tissue repair process. Aspirin induces and acetylates COX-2 to produce 15-(R)-epi-lipoxinA4, an anti-inflammatory mediator thought to protect the gastric mucosa against aspirin-induced injury. Recently, three different PGE synthases have been identified, that convert COX-2 metabolites into PGE2. mPGE synthase (mPGES)-1 has been shown to be inducible, and to colocalize with COX-2 in fibroblasts and macrophages infiltrating the gastric ulcer bed. cPGES and mPGES-2 have been found expressed in normal gastric mucosa, with no change in expression levels seen in gastritis or gastric ulcer tissue. Finally, this review discusses the role of these enzymes in the pathophysiology of the gastric mucosa, as well as the biologcal significance of their inhibition.

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Irritant-induced cyclooxygenase-2 is involved in the defense mechanism of the gastric mucosa in mice

Abstract: Pretreatment-induced COX-2, in addition to COX-1, seemed to be involved in the defense mechanism through minimizing the damage caused by a subsequent irritant.

Cited by 11 publications

References 30 publications

Protective role of adiponectin against ethanol-induced gastric injury in mice

Protective role of adiponectin against ethanol-induced gastric injury in mice

Host-specific differences in the physiology of acid secretion related to prostaglandins may play a role in gastric inflammation and injury

The Role of Cyclooxygenase in Gastric Mucosal Protection

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