Esophageal Epithelial Resistance and Lower Esophageal Sphincter Muscle Contraction Increase in a Chronic Diabetic Rabbit Model

Capanoglu, Doga; Coskunsever, Deniz; Olukman, Murat; Ülker, Sibel; Bor, Serhat

doi:10.1007/s10620-016-4111-8

Cited by 3 publications

(1 citation statement)

References 21 publications

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“…Many comprehensive studies of the morphological and electrophysiological changes of the esophagus exposed to acidic pH and pepsin were performed in rabbits [4]. Long-term exposure to acids and pepsin dilates the intercellular spaces in the esophageal mucosa.…”

Section: Resultsmentioning

confidence: 99%

Response of Esophageal Epithelium to Acute and Chronic Stress in Rabbits

Ergün¹,

Capanoglu²,

Kıpçak

et al. 2021

Bull Exp Biol Med

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We studied electrophysiological changes in rabbit esophageal epithelium following acute (AS) and chronic stress (CS). Esophageal tissue was placed in Ussing chamber and the potential difference U between the luminal and abluminal sides, the short-circuit current I sc , as well as the tissue resistance R were measured. The initial values of these parameters for each sample were determined after the samples were stabilized in Ringer solution. Then, the tissues were exposed for 1 h to normal Ringer solution or Ringer solution with pH 4.0 and pH 1.7 with or without pepsin (0.25 mg/ml). Fluorescein was added to the luminal side of the sample to measure its permeability. In the AS group, U at Ringer solution (pH 1.7)+pepsin was significantly decreased in comparison with the baseline and control values (by 46 and 22%, respectively, p<0.05). R decreased by 74% in comparison with baseline, which little differed from the decrease in control samples exposed to Ringer solution (pH 1.7)+pepsin (by 62%). CS did not change U relative to baseline values, while changes in R were similar to those in the AS group. In the AS group, the permeability of the esophageal tissue perfused with Ringer solution (pH 1.7)+pepsin was significantly higher than in both the control and CS groups. AS, but not CS, made the esophageal epithelium more sensitive to the effects of noxious agents, disrupted barrier properties, and increased permeability. The effects of stress on gastroesophageal reflux disease symptoms can be related to severe exposure to acid and/or pepsin; however, the mechanisms other than epithelial defense should be evaluated.

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Section: Resultsmentioning

confidence: 99%

Response of Esophageal Epithelium to Acute and Chronic Stress in Rabbits

Ergün¹,

Capanoglu²,

Kıpçak

et al. 2021

Bull Exp Biol Med

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Lubiprostone protects esophageal mucosa from acid injury in porcine esophagus

Krüger

Pridgen

Taylor

et al. 2020

American Journal of Physiology-Gastrointestinal and Liver Physi

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Esophageal injury from acid exposure related to gastroesophageal reflux disease is a common problem and a risk factor for development of Barrett’s esophagus and esophageal adenocarcinoma. Our previous work highlights the benefits of using porcine esophagus to study human esophageal disease because of the similarities between porcine and human esophagus. In particular, esophageal submucosal glands (ESMGs) are present in human esophagus and proximal porcine esophagus but not in rodent esophagus. Although CFTR is expressed in the ducts of ESMGs, very little is known about CFTR and alternate anion channels, including ClC-2, in the setting of acid-related esophageal injury. After finding evidence of CFTR and ClC-2 in the basal layers of the squamous epithelium, and in the ducts of the ESMGs, we developed an ex vivo porcine model of esophageal acid injury. In this model, esophageal tissue was placed in Ussing chambers to determine the effect of pretreatment with the ClC-2 agonist lubiprostone on tissue damage related to acid exposure. Pretreatment with lubiprostone significantly reduced the level of acid injury and significantly augmented the recovery of the injured tissue ( P < 0.05). Evaluation of the interepithelial tight junctions showed well-defined membrane localization of occludin in lubiprostone-treated injured tissues. Pretreatment of tissues with the Na+-K+-2Cl− cotransporter inhibitor bumetanide blocked lubiprostone-induced increases in short-circuit current and inhibited the reparative effect of lubiprostone. Furthermore, inhibition of ClC-2 with ZnCl2 blocked the effects of lubiprostone. We conclude that ClC-2 contributes to esophageal protection from acid exposure, potentially offering a new therapeutic target. NEW & NOTEWORTHY This research is the first to describe the presence of anion channels ClC-2 and CFTR localized to the basal epithelia of porcine esophageal mucosa and the esophageal submucosal glands. In the setting of ex vivo acid exposure, the ClC-2 agonist lubiprostone reduced acid-related injury and enhanced recovery of the epithelial barrier. This work may ultimately provide an alternate mechanism for treating gastroesophageal reflux disease.

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UegWeek 2020 Poster Presentations

2020

UEG Journal

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Esophageal Epithelial Resistance and Lower Esophageal Sphincter Muscle Contraction Increase in a Chronic Diabetic Rabbit Model

Cited by 3 publications

References 21 publications

Response of Esophageal Epithelium to Acute and Chronic Stress in Rabbits

Response of Esophageal Epithelium to Acute and Chronic Stress in Rabbits

Lubiprostone protects esophageal mucosa from acid injury in porcine esophagus

UegWeek 2020 Poster Presentations

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