Studies of Esophageal Epithelial Cell Proliferation in Patients with Reflux Esophagitis

Bile Acid Promotes the Proliferation of Squamous Cell Carcinoma of the Esophagus, Independent of its Inducing COX-2 Expression

“…In the current study, the proliferation of every esophageal cancer cell line was stimulated at a low dose of CDCA (around 30 M), which is compatible with the bile acid concentration in patients with minimal mucosal change. Interestingly, hyperproliferation of the squamous epithelium is one of the histological characteristics of minimal mucosal changes of the esophagus [29]. In the present study, we used unconjugated chenodeoxycholic acid (CDCA), because primary bile acid (cholic acid, CDCA) is the more dominant component in the esophageal reflux contents than secondary bile acid (deoxycholic acid, lithocolic acid, and so forth) [30].…”

Taxol toxicity. Epithelial necrosis in the gastrointestinal tract associated with polymerized microtubule accumulation and mitotic arrest

“…Gastroesophageal reflux is known to increase the mitotic rate of the esophageal epithelium. 22 An increase in mitotic rate would be expected to predispose the epithelium to the toxic effects of taxol. This may be a vicious circle, because one of the side effects of taxol is nausea and vomiting.…”

Impact of Gastro-esophageal Reflux on Mucin mRNA Expression in the Esophageal Mucosa

“…Hyperplasia of the basal cell of the esophageal mucosa is also evident in patients with gastro-esophageal reflux, and it is probably caused by epithelial repair mechanisms in response to reflux-induced damage. 14 The presence of CK-14 has been shown to be restricted to the basal cell layer within the esophageal mucosa, and hyperplasia of this layer is associated with increased expression. 15,16 Hence, we evaluated CK-14 as another potential surrogate tissue marker of reflux.…”

“…When examining the mucosal biopsy specimens, we also evaluated IL-6 mRNA expression, as this has previously been shown to correlate with reflux-induced mucosal inflammation, [11][12][13] and we evaluated CK-14 mRNA expression, an increase of which has been shown to correlate with hyperplasia of the basal cell layer of the esophageal mucosa, i.e., one of the earliest reflux-induced histopathological changes. [14][15][16] Cell Culture and Acid/Bile Treatment The HET-1A cell line was used to model the response of normal human esophageal epithelium to acid and/or bile exposure. This is a keratinocyte cell line that was derived from the esophagus of a human male and then immortalized with SV-40 large T antigen.…”