Effect of Helicobacter pylori on Tight Junctions in Gastric Epithelia
| Autor: | Carlos Abraham García-García, Luis Felipe Montano Estrada, Erika P. Rendón-Huerta |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
03 medical and health sciences 030104 developmental biology 0302 clinical medicine biology Tight junction 030220 oncology & carcinogenesis InformationSystems_INFORMATIONSTORAGEANDRETRIEVAL Helicobacter pylori biology.organism_classification GeneralLiterature_REFERENCE(e.g. dictionaries encyclopedias glossaries) Molecular biology |
| DOI: | 10.5772/intechopen.96607 |
| Popis: | Molecular complexes grouped under the names of tight, adherent or gap junction regulate the flow of water, ions and macromolecules through epithelium paracellular spaces. The main constituents of tight junctions are claudins, a family of 26 different proteins whose expression and distribution are tissue specific but varies in tumors. A change in claudin 1, 3, 4, 5, 6, 7, 9 and 18 expression, that contributes to lose epithelial cohesion, has been associated to enhanced cell proliferation, migration, and invasiveness in gastric neoplastic tissue. Chronic inflammation process induced by H. pylori infection, a major risk factor for gastric cancer development, disrupts tight junctions via CagA gene, Cag pathogenicity island, and VacA, but the effect upon the epithelial barrier of H. pylori lipopolysaccharides or H. pylori-induced up-regulation of mTOR and ERK signaling pathways by microRNA-100 establishes new concepts of proof. |
| Databáze: | OpenAIRE |
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