[Cytoprotective effects of heat shock protein-70 in bronchial epithelium against neutrophil elastase-induced cell injury].

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  • Additional Information
    • Source:
      Publisher: Nihon Allergy Gakkai Country of Publication: Japan NLM ID: 0241212 Publication Model: Print Cited Medium: Print ISSN: 0021-4884 (Print) Linking ISSN: 00214884 NLM ISO Abbreviation: Arerugi Subsets: MEDLINE
    • Publication Information:
      Publication: Tokyo : Nihon Allergy Gakkai
      Original Publication: Tokyo, Nippon Arerugi Gakkai.
    • Subject Terms:
      Bronchi/*physiology ; HSP70 Heat-Shock Proteins/*physiology ; Leukocyte Elastase/*physiology; Bronchi/chemistry ; Cells, Cultured ; Epithelial Cells/chemistry ; Epithelial Cells/physiology ; HSP70 Heat-Shock Proteins/analysis ; Humans
    • Abstract:
      Background: Neutrophil releases several mediators during inflammation, including neutrophil elastase (NE) that impairs bronchial epithelial function. The stress response and stress proteins protect cells against a variety of cytotoxic conditions. Accordingly, we tested the hypothesis that bronchial epithelial heat shock protein (Hsp-70) would protect a NE-induced cell injury.
      Methods: Bronchial epithelial cells (BECs) obtained by bronchial brushing under bronchoscopy were cultured and used for experiments. Expression of Hsp-70 in BECs was confirmed by Western blot and flowcytometric analysis. To test Hsp-70 in BECs, induction of Hsp-70 protein into BECs was carried out by liposome-based delivery system. Introduction of Hsp-70 into BECs were examined by direct fluorescence microscope examination and flowcytometric analysis. NE-induced cytotoxicity was evaluated by cell culture supernatant LDH assay and cell detachment assay.
      Results: Higher expressions of Hsp-70 were observed in BECs, which were induced by sodium arsenite. Over expression of Hsp-70 in BECs reduced NE-induced cell injury. Introduction of Hsp-70 protein into BECs by liposomal delivery decreased LDH release, and inhibited necrosis and apoptosis of the cells by NE as compared to untreated control.
      Conclusion: These data suggested that Hsp-70 in BECs may inhibit NE-induced airway epithelial damage. Liposomal delivery of Hsp-70 into BECs may be a possible means of protecting bronchial epithelium against inflammatory airway diseases including acute and chronic bronchitis.
    • Accession Number:
      0 (HSP70 Heat-Shock Proteins)
      EC 3.4.21.37 (Leukocyte Elastase)
    • Publication Date:
      Date Created: 20060803 Date Completed: 20060915 Latest Revision: 20061115
    • Publication Date:
      20240829
    • Accession Number:
      16883109