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    Interferon-gamma sensitizes colonic epithelial cell lines to physiological and therapeutic inducers of colonocyte apoptosis.

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    Authors
    O'Connell, J
    Bennett, M W
    Nally, K
    O'Sullivan, G C
    Collins, J K
    Shanahan, F
    Affiliation
    Department of Medicine, Cork University Hospital, National University of Ireland,, Cork, Ireland. j.oconnell@ucc.ie
    Issue Date
    2012-02-03T15:12:20Z
    MeSH
    Antineoplastic Agents/*pharmacology
    Apoptosis/*drug effects
    Cell Line
    Colon/drug effects/*pathology
    Drug Synergism
    Fas Ligand Protein
    Fatty Acids, Volatile/pharmacology
    Humans
    Interferon-gamma/*pharmacology
    Intestinal Mucosa/drug effects/*pathology
    Membrane Glycoproteins/pharmacology
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    Citation
    J Cell Physiol. 2000 Dec;185(3):331-8.
    Journal
    Journal of cellular physiology
    URI
    http://hdl.handle.net/10147/209102
    DOI
    10.1002/1097-4652(200012)185:3<331::AID-JCP3>3.0.CO;2-V
    PubMed ID
    11056003
    Abstract
    Homeostasis in the colonic epithelium is achieved by a continuous cycle of proliferation and apoptosis, in which imbalances are associated with disease. Inflammatory bowel disease (IBD) and colon cancer are associated with either excessive or insufficient apoptosis of colonic epithelial cells, respectively. By using two colonic epithelial cell lines, HT29 and SW620, we investigated how the epithelial cell's sensitivity to apoptosis was regulated by the proinflammatory cytokine interferon-gamma (IFN-gamma). We found that IFN-gamma sensitized HT29 cells, and to a lesser extent SW620, to diverse inducers of apoptosis of physiologic or therapeutic relevance to the colon. These apoptosis inducers included Fas (CD95/APO-1) ligand (FasL), short-chain fatty acids, and chemotherapeutic drugs. The extent of IFN-gamma-mediated apoptosis sensitization in these two cell lines correlated well with the degree of IFN-gamma-mediated upregulation of the proapoptotic protease caspase-1. Although IFN-gamma alone effectively sensitized HT29 cells to apoptosis, inclusion of the protein synthesis inhibitor cyclohexamide (CHX) during apoptotic challenge was necessary for maximal sensitization of SW620. The requirement of CHX to sensitize SW620 cells to apoptosis implies a need to inhibit translation of antiapoptotic proteins absent from HT29. In particular, the antiapoptotic protein Bcl-2 was strongly expressed in SW620 cells but absent from HT29. Our results indicate that IFN-gamma increases the sensitivity of colonic epithelial cells to diverse apoptotic stimuli in concert, via upregulation of caspase-1. Our findings implicate caspase-1 and Bcl-2 as important central points of control determining the general sensitivity of colonic epithelial cells to apoptosis.
    Language
    eng
    ISSN
    0021-9541 (Print)
    0021-9541 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1002/1097-4652(200012)185:3<331::AID-JCP3>3.0.CO;2-V
    Scopus Count
    Collections
    Cork University Hospital

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