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Commentary on “Bile Salts Differentially Sensitize Esophageal Squamous Cells to CD95 (Fas/Apo-1 Receptor) Mediated Apoptosis”

      Drs. Naran, Abrams, de Oliveira, and Hughes of the Section of Gastrointestinal Surgery, Department of Surgery at the University of Pittsburgh have evaluated the role of non-acidic reflux and the molecular impact of the reflux contents to establish pathophysiologically the Barrett's esophagus [
      • Naran S.
      • Abrams P.
      • de Oliveira P.Q.
      • et al.
      Bile salts differentially sensitize esophageal squamous cells to CD95 (Fas/Apo-1 receptor) mediated apoptosis.
      ]. Of primacy to the hypothesis, the authors established the role of bile salts to elicit subsequent alterations in cell surface expression of CD95 (Fas/Apo-1). The authors further explored the differential of the normal esophageal squamous epithelium versus that of Barrett's columnar epithelium to sensitivity of CD95-mediated apoptosis. In the article recently published in the Journal of Surgical Research [
      • Naran S.
      • Abrams P.
      • de Oliveira P.Q.
      • et al.
      Bile salts differentially sensitize esophageal squamous cells to CD95 (Fas/Apo-1 receptor) mediated apoptosis.
      ], the authors note that bile salt exposure sensitizes esophageal squamous cells to CD95-mediated apoptosis. Of key differentiation, this response is differentiated from that of normal columnar epithelial cells and, thus, may be hypothetically indicative of the pathogenesis of the Barrett's esophagus.
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