Bile Exposure Inhibits Expression of Squamous Differentiation Genes in Human Esophageal Epithelial Cells

Reveiller, Marie; Ghatak, Sayak; Toia, Liana; Kalatskaya, Irina; Stein, Lincoln; D’Souza, Mary; Zhou, Zhongren; Bandla, Santhoshi; Gooding, William E.; Godfrey, Tony E.; Peters, Jeffrey H.

doi:10.1097/sla.0b013e3182512af9

Cited by 17 publications

(18 citation statements)

References 42 publications

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“…Bile plays a role with refluxed acid in the development of Barrett's esophagus and its malignant transformation, according to Peters and colleagues [5]. In our case, visual evidence of bile staining had disappeared two months later ( Figure 6).…”

Section: Discussionmentioning

confidence: 63%

Biliary Esophagitis: A Case Report

Demos¹,

Agams²,

Becker³

2017

J Gastrointest Dig Syst

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Section: Discussionmentioning

confidence: 63%

Biliary Esophagitis: A Case Report

Demos¹,

Agams²,

Becker³

2017

J Gastrointest Dig Syst

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“…According to the literature, AC reflux is not the only factor that has an important role in the pathogenesis of BE . Recent study suggests that bile has more dramatic effect than acid on inhibition of proliferation and on the squamous differentiation of the esophageal cells . It was discovered that alkaline reflux may also damage normal esophageal epithelium.…”

Section: Discussionmentioning

confidence: 99%

Activity of mitogen-activated protein kinases in the esophageal epithelium of patients with Barrett's esophagus

et al. 2014

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Barrett's esophagus (BE), a complication of gastroesophageal reflux disease, is associated with an increased risk of esophageal cancer. Mitogen-activated protein kinases may play an important role in the pathogenesis of this process. We aimed to evaluate mitogen-activated protein kinases activity in esophageal mucosa of patients with BE and find possible relationship between reflux type and BE. Twenty-four patients (mean age: 59 years) with gastroesophageal reflux disease symptoms and endoscopically suspected esophageal metaplasia (ESEM) were prospectively enrolled for testing by a multichannel intraluminal impedance monitoring along with a Bilitec 2000. Endoscopic biopsies were taken from methylene blue-positive pit patterns (sites suggesting specialized intestinal metaplasia [SIM]), from 2 cm above the Z-line and from cardial parts of the stomach. The biopsies were analyzed for extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 activity by Western blot. Seventeen ESEMs had histologically proven metaplasia: eight patients had SIM and nine had gastric-type epithelia (GE). Biliary reflux was more evident in SIM (P = 0.019) but not in GE (P = 0.019); non-biliary reflux was typical for GE (P = 0.005) but not for SIM (P = 0.04). Strong activations of ERK and p38 were found predominantly in SIM, but not in normal esophageal mucosa (NE) (P = 0.01 and P < 0.001 respectively). Strong signals for active JNK and p38 were detected in GE, but not in NE (P = 0.006 and P = 0.02 respectively). ERK activity was significantly higher than p38 activity in ESEM patients only with GE (P = 0.02). The strong activation of ERK, but not JNK is indicative of SIM. The presence of bile in gastroesophageal refluxate is predisposing to SIM, but not to GE in esophageal mucosa.

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“…W e read with interest the article by Reveiller et al, 1 which was published in a recent issue of the Annals of Surgery. The genetic studies compared the effects of bile and acid on squamous and columnar epithelial cells of the esophagus, thus remodeling gastroesophageal reflux disease at the cellular level.…”

Section: To the Editormentioning

confidence: 98%

“…As a consequence, the bile acid induced genetic changes favoring the activation of the CDx2 pathway and mediating the development of premalignant Barrett's esophagus. 1 Thus it seems that the bile-milieu formats the cellular type toward Barrett's esophagus. Remains to be questioned the clinical relevance of these striking and important findings.…”

Section: To the Editormentioning

confidence: 99%

“…The authors found that the major compounds of reflux, that is, bile and acid, affect the genetic program of esophageal epithelial cells. 1 Most importantly, bile acids inhibited the genetic program required for the differentiation of normal squamous epithelial cells. As a consequence, the bile acid induced genetic changes favoring the activation of the CDx2 pathway and mediating the development of premalignant Barrett's esophagus.…”

Section: To the Editormentioning

confidence: 99%

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