Abstract
Helicobacter pylori infection is a crucial factor in the pathogenesis of several digestive disorders, including peptic ulcers, chronic gastritis, and gastric cancer. Moreover H. pylori induces disease-specific protein expression in gastric epithelial cells. The aim of the present study was to characterize proteins differentially expressed in H. pylori-infected gastric epithelial AGS cells. An in vitro model was established using a multiplicity of infection of 100 and evaluating the effectiveness of H. pylori infection by functional analyses. Changes in protein patterns were identified using a proteomic approach consisting of two-dimensional fluorescence difference gel electrophoresis and mass spectrometry. The expression of many proteins was found to be altered, and 28 of these were identified and classified as protein synthesis- and folding-related proteins, cytoskeleton proteins, metabolic enzymes, transcription- and translation-related proteins, angiogenesis/metastasis-related proteins, cell communication/signal transduction-related proteins, or others (oxygen-regulated protein and oncoprotein). The expression profiles of eight of these proteins, laminin gamma-1 chain precursor, valosin-containing protein, heat shock 70-kDa protein, mitochondrial matrix protein P1, FK506-binding protein 4, T-complex protein 1, enolase alpha, and 14-3-3 beta were further examined in cancerous and paired surrounding normal tissues by immunoblot assay and immunohistochemical staining to identify molecular targets that may be involved in the pathogenesis of H. pylori-induced gastric diseases. On the basis of our results, valosin-containing protein, mitochondrial matrix protein P1, T-complex protein 1, enolase alpha, and 14-3-3 beta may play a crucial role in H. pylori-induced gastric carcinogenesis by mediating antiapoptotic and proliferative responses.
Highlights
Helicobacter pylori infection is a crucial factor in the pathogenesis of several digestive disorders, including peptic ulcers, chronic gastritis, and gastric cancer
Induction of the Scattering Phenotype, IL-8 Release, and COX-2 Protein Expression in AGS Cells following H. pylori Infection—To study H. pylori pathogenesis in vitro, AGS gastric epithelial cells were infected with H. pylori, and infection was monitored by the appearance of the scattering hummingbird phenotype
ELISA showed that IL-8 levels in the medium were 34.4 Ϯ 12.9 pg/ml for noninfected cells and 1,118.3 Ϯ 47.4 pg/ml for cells infected with H. pylori for 24 h (Fig. 1B), whereas immunoblot analysis showed that COX-2 expression was induced in H. pyloriinfected cells after 24 h (Fig. 1C)
Summary
Helicobacter pylori infection is a crucial factor in the pathogenesis of several digestive disorders, including peptic ulcers, chronic gastritis, and gastric cancer. H. pylori induces disease-specific protein expression in gastric epithelial cells. The aim of the present study was to characterize proteins differentially expressed in H. pylori-infected gastric epithelial AGS cells. Helicobacter pylori infects about 50% of the world’s population and has been shown to be an important pathogen in several digestive disorders, such as peptic ulcers, chronic gastritis, and gastric cancer [1]. Microarray analysis of gene expression induced by H. pylori in AGS cells showed marked changes in ϳ200 genes, and the up-regulation of c-jun, jun-B, c-fos, and cyclin D1 was confirmed by RT-PCR analysis [14]. Changes in the protein profile of host cells infected with H. pylori have not been investigated extensively
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