Correlation of Probe-Based Confocal Laser Endomicroscopy (pCLE) and Mucosal Integrity Testing (MIT) with Epithelial Barrier Function and Presence of Gastroesophageal Reflux Disease (GERD).

Introduction: Epithelial barrier function (EBF) disruption is a key mechanism underlying gastroesophageal reflux disease (GERD). Our aim was to assess whether two novel technologies, probe-based confocal laser endomicroscopy (pCLE) and mucosal integrity testing (MIT), could assess EBF.

Methods: We prospectively enrolled patients undergoing upper endoscopy for refractory GERD or non-GERD conditions.

Gastric secretion.

Purpose Of Review: The review summarizes the past year's literature, basic science and clinical, regarding the neural, paracrine, hormonal, and intracellular regulation of gastric acid secretion.

Recent Findings: Gastric acid facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B(12), and certain medications (e.g.

H. pylori acutely inhibits gastric secretion by activating CGRP sensory neurons coupled to stimulation of somatostatin and inhibition of histamine secretion.

Acute Helicobacter pylori infection produces hypochlorhydria. The decrease in acid facilitates survival of the bacterium and its colonization of the stomach. The present study was designed to identify the pathways in oxyntic mucosa by which acute H.

Gastric secretion.

Purpose Of Review: This review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion, both basic science and clinical.

Recent Findings: Gastric acid secretion facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B12, and certain medications as well as prevents bacterial overgrowth, enteric infection, and possibly community-acquired pneumonia, spontaneous bacterial peritonitis, and IgE-mediated food allergy. It is regulated by neural (e.

Transcriptional regulation by post-transcriptional modification--role of phosphorylation in Sp1 transcriptional activity.

Sp1 is a ubiquitously expressed transcription factor involved in the regulation of a large number of genes including housekeeping genes as well as actively regulated genes. Although Sp1 was discovered nearly three decades ago, its functional diversity is still not completely understood. One of the ways that make Sp1 versatile in transcriptional regulation is its post-transcriptional modification, which alters Sp1 structure in different cells and at different times.

ENaC alpha-subunit variants are expressed in lung epithelial cells and are suppressed by oxidative stress.

Amiloride-sensitive epithelial sodium channel (ENaC) is a major sodium channel in the lung facilitating fluid absorption. ENaC is composed of alpha-, beta-, and gamma-subunits, and the alpha-subunit is indispensable for ENaC function in the lung. In human lungs, the alpha-subunit is expressed as various splice variants.

Poly(ADP-ribose) polymerase-1 regulates vimentin expression in lung cancer cells.

Vimentin is one of the mammalian intermediate filament proteins. It is expressed in cells of mesenchymal origin and is characteristic of proliferating cells at the fetal stage. During malignancy, vimentin expression is activated in certain lung epithelial cells.

Identification of a hydrogen peroxide-induced PP1-JNK1-Sp1 signaling pathway for gene regulation.

Oxidative stress often results in changes in gene expression through the regulation of transcription factors. In this study, we examine how Sp1 phosphorylation is regulated by H(2)O(2) in a human alveolar epithelial cell line (HAE). Treatment of HAE cells with H(2)O(2) increases phosphorylation of Sp1 and activates JNK.

Sp1: regulation of gene expression by phosphorylation.

As the prototype of a family of transcription factors, Sp1 has been extensively studied and widely reported for its role in gene regulation. The first evidence of Sp1 phosphorylation was reported more than a decade ago. Since then, an increasing number of Sp1 phosphorylation events have been characterized.

Interferon-gamma regulates ClC-2 chloride channel in lung epithelial cells.

Epithelial Cl(-) channels mediate Cl(-) and fluid secretion in the lung. In cystic fibrosis, aberrant Cl(-) secretion is one of the major causes for lung fluid imbalance. Regulation of Cl(-) channels is therefore an important issue in the lung.

Modulation of Sp1 and Sp3 in lung epithelial cells regulates ClC-2 chloride channel expression.

ClC-2 is a pH- and voltage-activated chloride channel, which is highly expressed in fetal airways and downregulated at birth. The ClC-2 promoter contains consensus binding sites within the first 237 bp, which bind transcription factors Sp1 and Sp3(1). This study directly links Sp1 and Sp3 with ClC-2 protein expression by demonstrating: (i) induction of ClC-2 protein by transient overexpression of each transcription factor in adult rat Type II cells, which have low levels of ClC-2; and (ii) reduction of ClC-2 expression by incubation with a competitive inhibitor of Sp1 and Sp3 in fetal rat Type II cells, which have high levels of endogenous ClC-2.

Expression of alpha-ENaC2 is dependent on an upstream Sp1 binding motif and is modulated by protein phosphatase 1 in lung epithelial cells.

The amiloride-sensitive Na(+) channel ENaC is expressed in lung epithelium and plays a pivotal role in lung fluid clearance in the newborn. Multiple splice variants of the ENaC alpha-subunit have been reported. Among them, alpha-ENaC2 accounts for a considerable portion of alpha-ENaC transcripts in human lung and kidney, possesses channel functions similar to alpha-ENaC1, and is driven by a downstream promoter.