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Expression of inducible nitric oxide synthase and elevation of tyrosine nitration of a 32-kilodalton cellular protein in brain capillary endothelial cells from rats infected with a neuropathogenic murine leukemia virus

  1. Author:
    Jinno-Oue, A.
    Wilt, S. G.
    Hanson, C.
    Dugger, N. V.
    Hoffman, P. M.
    Masuda, M.
    Ruscetti, S. K.

  2. Author Address

    NCI, Basic Res Lab, Bldg 469,Room 205, Frederick, MD 21702 USA NCI, Basic Res Lab, Frederick, MD 21702 USA Univ Maryland, Res Serv, Dept Vet Affairs Med Ctr, Baltimore, MD 21201 USA Univ Maryland, Dept Neurol, Baltimore, MD 21201 USA Dokkyo Univ, Sch Med, Dept Microbiol, Mibu, Tochigi 3210293, Japan Ruscetti SK NCI, Basic Res Lab, Bldg 469,Room 205, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Journal of Virology
    1. 77
    2. 9
    3. Pages: 5145-5151
  4. Type of Article: Article
  1. Abstract:

    PVC-211 murine leukemia virus (MuLV) is a neuropathogenic variant of Friend MuLV (F-MuLV) which causes a rapidly progressive spongiform neurodegenerative disease in rodents. The primary target of PVC-211 MuLV infection in the brain is the brain capillary endothelial cell (BCEC), which is resistant to F-MuLV infection. Previous studies have shown that changes in the envelope gene of PVC-211 MuLV confer BCEC tropism to the virus. However, little is known about how infection of BCECs by PVC-211 MuLV induces neurological disease. Previous results suggest that nitric oxide (NO), which has been implicated as a potential neurotoxin, is involved in PVC-211 MuLV-induced neurodegeneration. In this study, we show that expression of inducible nitric oxide synthase (iNOS), which produces NO from L-arginine, is induced in BCECs from PVC-211 MuLV-infected rats. Furthermore, elevated levels of a 32-kDa cellular protein modified by 3-nitrotyrosine, which is a hallmark of NO production, were observed in virus-infected BCECs. BCECs from rats infected with BCEC-tropic but nonneuropathogenic PVF-e5 MuLV; which is a chimeric virus between PVC-211 MuLV and F- MuLV, fail to induce either iNOS expression or elevation of tyrosine nitration of a 32-kDa protein. These results suggest that expression of iNOS and nitration of tyrosine residues of a 32-kDa protein in PVC-211 MuLV-infected BCECs may play an important role in neurological disease induction.

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