Factors influencing intercellular spaces in the rat esophageal epithelium

Zhang, Donghong; Zhou, Liya; Xiuyun, Dong; Cui, Rong; Xue, Yan; Lin, San-ren

doi:10.3748/wjg.v16.i9.1063

Cited by 15 publications

(19 citation statements)

References 36 publications

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“…Using electron microscopy, we confirmed the widening of the intercellular spaces of the esophageal epithelia in the SB, SS, and SG in the RE group in comparison with the control group, as previously reported (Farré et al, 2007;Miwa et al, 2009;Ito et al, 2010;Zhang et al, 2010). This result suggests that the esophageal epithelia in rat RE models were affected by acid reflux, which is consistent with previous reports.…”

Section: Discussionsupporting

confidence: 91%

<b>Ultrastructural analyses of the rat esophageal stratified epithelium under normal conditions and in chronic reflux esophagitis </b>

Mori

Koike

Gotow

et al. 2011

Archives of Histology and Cytology

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TJ structures only in the stratum granulosum (SG) of the esophageal epithelia in control rats, and the number of TJ structures seemed to be decreased in the RE model.Most of the TJs were composed of only one ＂kissing point.＂ Freeze-fracture electron microscopy did not allow identification of typical TJ strands, suggesting that TJs in the rat esophageal mucosa were not well-developed. Immunoelectron microscopy confirmed our previous immunohistochemical results indicating that claudin-3 was located on the surface of esophageal epithelial cells in control rats and that the immunoreactivity decreased in the RE group. However, claudin-3 was diffusely localized on the plasma membrane and not concentrated on the TJ structures. These results indicate that claudin-3 is not directly involved in the composition of the TJ structure.

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Section: Discussionsupporting

confidence: 91%

<b>Ultrastructural analyses of the rat esophageal stratified epithelium under normal conditions and in chronic reflux esophagitis </b>

Mori

Koike

Gotow

et al. 2011

Archives of Histology and Cytology

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“…Animal studies regarding reflux esophagitis induced by esophagoduodenostomy reveal that the earliest sign of esophageal inflammation is an infiltration of the submucosa by white cells that is cytokine-mediated and precedes the development of surface lesions by weeks [7]. This immune system response is supported by transmission electron microscopy, which showed no evidence of inflammation in the esophageal mucosa in response to acute stress, hydrochloric acid, ethanol, aspirin or prednisolone [8].…”

supporting

confidence: 52%

Could proton pump inhibitors cause cancer?

Rösch

2014

Expert Review of Clinical Pharmacology

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“…It has been shown that aspirin makes the esophageal mucosa more sensitive to the injurious action of acid and pepsin (44). In another study, intragastric administration of aspirin induced dilated intercellular spaces in the rat esophageal epithelium (45). In addition, some studies have observed that treatment with high doses of ASA provokes both significantly increased production of reactive oxygen species (ROS) (46) and inhibition of ROS scavenger activity (47).…”

Section: Discussionmentioning

confidence: 99%

Effect of aspirin treatment on the prevention of esophageal adenocarcinoma in a rat experimental model

et al. 2014

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Abstract. Aspirin has been proposed in recent years as a candidate for chemoprevention of adenocarcinoma in patients with Barrett's esophagus. The aim of the present study was to evaluate the effect of acetylsalicylic acid (ASA) in an experimental model of esophageal adenocarcinoma. An animal model of gastroenteroesophageal reflux was established using Wistar rats undergoing esophagojejunostomy with gastric preservation. Following surgery, rats were divided into three groups: i) control (vehicle); ii) ASA 50 mg/kg/day; and iii) ASA 5 mg/kg/day. Four months after surgery, the surviving animals were sacrificed and the rat esophagi were assessed for histological and biochemical [prostaglandin E 2 (PGE 2 ) and lipoxin A 4 (LXA 4 ) levels] analysis. As in the control rats, those receiving aspirin treatment showed no decrease in inflammation grade, extent of ulcerated esophageal mucosa, length of intestinal metaplasia in continuity with anastomosis, presence of intestinal metaplasia beyond anastomosis, severity of dysplasia or incidence of adenocarcinoma. In contrast, aspirin-treated rats showed decreased esophageal tissue levels of PGE 2 and increased LXA 4 , significantly in the high-dose aspirin group (P=0.008 and P=0.01, respectively). In this rat model of gastroesophageal reflux, the administration of aspirin modified esophageal tissue levels of PGE 2 and LXA 4 , but was not effective in preventing the development of esophageal adenocarcinoma.

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Factors influencing intercellular spaces in the rat esophageal epithelium

Abstract: Acute stress and aspirin can induce DIS of the esophageal epithelium in rats, and it is not correlated with acid reflux.

Cited by 15 publications

References 36 publications

<b>Ultrastructural analyses of the rat esophageal stratified epithelium under normal conditions and in chronic reflux esophagitis </b>

<b>Ultrastructural analyses of the rat esophageal stratified epithelium under normal conditions and in chronic reflux esophagitis </b>

Could proton pump inhibitors cause cancer?

Effect of aspirin treatment on the prevention of esophageal adenocarcinoma in a rat experimental model

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