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    Bcl-w is an important determinant of damage-induced apoptosis in epithelia of small and large intestine.

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    Authors
    Pritchard, D Mark
    Print, C
    O'Reilly, L
    Adams, J M
    Potten, Christopher S
    Hickman, John A
    Affiliation
    CRC Department of Epithelial Biology, Paterson Institute, Christie Hospital NHS Trust, Manchester, UK.
    Issue Date
    2000-08-10
    
    Metadata
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    Abstract
    The potential role of the bcl-2 relative bcl-w as a physiological regulator of apoptosis in intestinal epithelia has been investigated. Immunoblots for bcl-w with new monoclonal antibodies revealed that it was expressed in the small intestine and colon, among other murine tissues, as well as in six human tumour cell lines of epithelial origin, including two colon carcinoma lines. To assess whether bcl-w regulates either spontaneous or damage-induced apoptosis in the small intestine or colon, apoptosis in intestinal crypts of bcl-w -/- and wild-type mice was quantified microscopically on a cell positional basis. Spontaneous apoptosis within crypt epithelia was not significantly increased by loss of bcl-w, in either the small intestine or midcolon. However, after treatment with the cytotoxic drug 5-fluorouracil or with gamma-radiation, the bcl-w-null animals exhibited substantially more apoptosis than their wild-type counterparts in both tissues. The greatest enhancement of apoptosis attributable to the absence of bcl-w (up to sixfold) occurred in the small intestine. Hence, bcl-w is an important determinant of damage-induced apoptosis in intestinal epithelia, and unlike bcl-2, which regulates only colonic apoptosis, plays a major role in small intestinal epithelium.
    Citation
    Bcl-w is an important determinant of damage-induced apoptosis in epithelia of small and large intestine. 2000, 19 (34):3955-9 Oncogene
    Journal
    Oncogene
    URI
    http://hdl.handle.net/10541/86184
    DOI
    10.1038/sj.onc.1203729
    PubMed ID
    10951589
    Type
    Article
    Language
    en
    ISSN
    0950-9232
    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.onc.1203729
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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