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    Anti-apoptotic effects of Z alpha1-antitrypsin in human bronchial epithelial cells.

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    Authors
    Greene, C M
    Miller, S D W
    Carroll, T P
    Oglesby, I K
    Ahmed, F
    O'Mahony, M
    Taggart, C C
    McElvaney, N G
    O'Neill, S J
    Affiliation
    Dept of Medicine Respiratory Research Division, RCSI Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. cmgreene@rcsi.ie
    Issue Date
    2010-05
    MeSH
    Adult
    Apoptosis
    Biopsy
    Blotting, Western
    Caspase 3
    Cell Line
    Cell Proliferation
    Emphysema
    Epithelial Cells
    Female
    Gene Expression
    Humans
    Immunoenzyme Techniques
    In Situ Nick-End Labeling
    Inhibitor of Apoptosis Proteins
    Male
    NF-kappa B
    Phosphorylation
    Respiratory Mucosa
    Reverse Transcriptase Polymerase Chain Reaction
    Up-Regulation
    alpha 1-Antitrypsin
    alpha 1-Antitrypsin Deficiency
    bcl-Associated Death Protein
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    Citation
    Anti-apoptotic effects of Z alpha1-antitrypsin in human bronchial epithelial cells. 2010, 35 (5):1155-63 Eur. Respir. J.
    Journal
    The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology
    URI
    http://hdl.handle.net/10147/127265
    DOI
    10.1183/09031936.00191908
    PubMed ID
    19840955
    Abstract
    alpha(1)-antitrypsin (alpha(1)-AT) deficiency is a genetic disease which manifests as early-onset emphysema or liver disease. Although the majority of alpha(1)-AT is produced by the liver, it is also produced by bronchial epithelial cells, amongst others, in the lung. Herein, we investigate the effects of mutant Z alpha(1)-AT (ZAAT) expression on apoptosis in a human bronchial epithelial cell line (16HBE14o-) and delineate the mechanisms involved. Control, M variant alpha(1)-AT (MAAT)- or ZAAT-expressing cells were assessed for apoptosis, caspase-3 activity, cell viability, phosphorylation of Bad, nuclear factor (NF)-kappaB activation and induced expression of a selection of pro- and anti-apoptotic genes. Expression of ZAAT in 16HBE14o- cells, like MAAT, inhibited basal and agonist-induced apoptosis. ZAAT expression also inhibited caspase-3 activity by 57% compared with control cells (p = 0.05) and was a more potent inhibitor than MAAT. Whilst ZAAT had no effect on the activity of Bad, its expression activated NF-kappaB-dependent gene expression above control or MAAT-expressing cells. In 16HBE14o- cells but not HEK293 cells, ZAAT upregulated expression of cIAP-1, an upstream regulator of NF-kappaB. cIAP1 expression was increased in ZAAT versus MAAT bronchial biopsies. The data suggest a novel mechanism by which ZAAT may promote human bronchial epithelial cell survival.
    Item Type
    Article
    Language
    en
    ISSN
    1399-3003
    ae974a485f413a2113503eed53cd6c53
    10.1183/09031936.00191908
    Scopus Count
    Collections
    Beaumont Hospital

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