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Transgenic expression in mouse lung reveals distinct biological roles for the adenovirus type 5 E1A 243-and 289-amino-acid proteins

  1. Author:
    Yang, Y. P.
    McKerlie, C.
    Borenstein, S. H.
    Lu, Z.
    Schito, M.
    Chamberlain, J. W.
    Buchwald, M.

  2. Author Address

    NCI, Mouse Canc Genet Program, Canc Res Ctr, Bldg 560,Room 32- 16,POB B, Frederick, MD 21702 USA Univ Toronto, Hosp Sick Children, Res Inst, Program Genet & Genom Biol, Toronto, ON M5G 1X8, Canada Univ Toronto, Hosp Sick Children, Res Inst, Program Immun Infect Injury & Repair, Toronto, ON M5G 1X8, Canada Univ Toronto, Dept Mol & Med Genet, Toronto, ON, Canada Univ Toronto, Dept Immunol, Toronto, ON, Canada Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada Sunnybrook & Womens Coll Hlth Sci Ctr, Mol & Cellular Biol Res Program, Toronto, ON, Canada Yang YP NCI, Mouse Canc Genet Program, Canc Res Ctr, Bldg 560,Room 32-16,POB B, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Journal of Virology
    1. 76
    2. 17
    3. Pages: 8910-8919
  4. Type of Article: Article
  1. Abstract:

    Little is known about the biological significance of human adenovirus type 5 (Ad5) E1A in vivo. However, Ads E1A is well defined in vitro and can be detected frequently in the lungs of patients with pulmonary disease. Transgenic expression of the Ads E1A gene targeted to the mouse lung reveals distinct biological effects caused by two Ads E1A products. Either of two Ads E1A proteins was preferentially expressed in vivo in the transgenic lungs. The preferential expression of the Ads E1A 243-amino-acid (aa) protein at a moderate level was associated with cellular hyperplasia, nodular lesions of proliferating lymphocyte-like cells, and a low level of p53- dependent apoptosis in the lungs of transgenic mice. In contrast, the preferential expression of the Ads E1A 289-aa protein at a moderate level resulted in a proapoptotic injury and an acute pulmonary proinflammation in the lungs of transgenic mice, mediated by multiple apoptotic pathways, as well as an enhancement of the host immune cell response. Expression of the Ads E1A 243-aa protein resulted in proliferation-stimulated p53 upregulation, while expression of the Ads E1A 289-aa protein led to DNA damage-induced p53 activation. These data suggest that the Ads E1A 243- and 289-aa proteins lead to distinct biological roles in vivo.

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