38 research outputs found
Barrett's esophagus: genetic and cell changes
Full text linkPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/86844/1/j.1749-6632.2011.06043.x.pd
579 Increased Expression, Secretion and Activation of IL-6 During the Neoplastic Progression of Barrett's Esophagus
No full textW1966 Unlike Deoxycholic Acid, Ursodeoxycholic Acid Does Not Cause DNA Damage or Activate the NF-κB Pathway in Barrett's Metaplasia In Vitro and In Vivo
No full textM1819 Exposure to Acid and Bile Salts Causes Esophageal Squamous Cells to Secrete Chemokines That Stimulate Immune Cell Migration
No full textW1881 In Neoplastic Barrett's Epithelial Cells, Esomeprazole Induces Apoptosis Through the Production of Reactive Oxygen Species: A Potential Role for PPIs in the Chemotherapy of Barrett's Cancer
No full text877 In Esophageal Squamous Epithelial Cell Lines From Patients With Eosinophilic Esophagitis (EoE), Omeprazole Blocks the Stimulated Secretion of Eotaxin-3: A Potential Anti-Inflammatory Effect of Omeprazole in EoE That is Independent of Acid Inhibition.
No full textIn Benign Barrett's Epithelial Cells, Acid Exposure Generates Reactive Oxygen Species That Cause DNA Double-Strand Breaks
No full text1063 Omeprazole Blocks Secretion of the Inflammatory Cytokine IL-8 in Esophageal Squamous Epithelial Cells Exposed to Acid and Bile Salts: A Potential Anti-Inflammatory Effect of PPIs Independent of Acid Inhibition
No full textUnlike Esophageal Squamous Cells, Barrett's Epithelial Cells Resist Apoptosis by Activating the Nuclear Factor-κB Pathway
No full textDifferences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus
No full textWe hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal squamous cells from patients with gastroesophageal reflux disease (GERD) with (NES-B3T) and without (NES-G2T) Barrett's esophagus and used those cells to study acid effects on MAPK proteins. During endoscopy in patients with GERD with and without Barrett's esophagus, we took biopsy specimens from the distal squamous esophagus to study MAPK proteins before and after esophageal perfusion with 0.1 N HCl. We used immunoblotting and Western blotting to study MEK1/2 phosphorylation at two activating sites (serines 217/221), MEK1 phosphorylation at an inhibitory site (threonine 286), and MEK1/2 activity. After acid exposure, both cell lines exhibited increased MEK1/2 phosphorylation at the activating sites; the NES-B3T cells had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the NES-G2T cells showed an acid-induced increase in MEK1/2 activity. Similarly, in the squamous epithelium of patients with GERD with and without Barrett's esophagus, acid perfusion increased MEK1/2 phosphorylation at the activating sites in both patient groups; the Barrett's patients had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the patients without Barrett's demonstrated an acid-induced increase in ERK1/2 phosphorylation. In esophageal squamous cell lines and biopsies from patients with GERD with and without Barrett's esophagus, we have found differences in MAPK pathways activated by acid exposure. We speculate that these differences might underlie the development of Barrett's metaplasia
