6533b7d8fe1ef96bd126a5ac

RESEARCH PRODUCT

Heat shock protein-27 protects human bronchial epithelial cells against oxidative stress-mediated apoptosis: possible implication in asthma.

André-patrick ArrigoJean BousquetAntonio M. VignolaMaria Assunta CostaGiuseppina ChiapparaAnna Maria MerendinoMario MelisVincenzo IzzoCatherine Paul

subject

Adultendocrine systemanimal structuresHSP27 Heat-Shock ProteinsInflammationApoptosisBronchiColumnar CellRespiratory MucosaBiologymedicine.disease_causeBiochemistryGene Expression Regulation EnzymologicHsp27Heat shock proteinmedicineBronchial BiopsyHumansHeat-Shock ProteinsEpithelial CellsCell BiologyHydrogen PeroxideOriginal ArticlesMiddle AgedOxidantsEpitheliumAsthmaCell biologyNeoplasm ProteinsOxidative Stressmedicine.anatomical_structureApoptosisImmunologybiology.proteinmedicine.symptomOxidative stressMolecular Chaperones

description

Inflammation of the human bronchial epithelium, as observed in asthmatics, is characterized by the selective death of the columnar epithelial cells, which desquamate from the basal cells. Tissue repair initiates from basal cells that resist inflammation. Here, we have evaluated the extent of apoptosis as well as the Hsp27 level of expression in epithelial cells from bronchial biopsy samples taken from normal and asthmatic subjects. Hsp27 is a chaperone whose expression protects against oxidative stress. We report that in asthmatic subjects the basal epithelium cells express a high level of Hsp27 but no apoptotic morphology. In contrast, apoptotic columnar cells are devoid of Hsp27 expression. Moreover, we observed a decreased resistance to hydrogen peroxide–induced apoptosis in human bronchial epithelial 16–HBE cells when they were genetically modified to express reduced levels of Hsp27.

https://pubmed.ncbi.nlm.nih.gov/12482203