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Article Dans Une Revue American Journal of Pathology Année : 1997

Transformation of rabbit vascular smooth muscle cells by human cytomegalovirus morphological transforming region I.

Alain Legrand
E.P Mayer
  • Fonction : Auteur
S Dalvi
  • Fonction : Auteur
M Nachtigal
  • Fonction : Auteur

Résumé

The association of human cytomegalovirus with atherosclerosis and the monoclonal hypothesis of atherogenesis suggested that transformation of vascular smooth muscle cells may be an outcome of the virus-host cell interaction. To test this hypothesis, rabbit aorta smooth muscle cells were transfected with the morphological transforming region I (mtrI) of human cytomegalovirus (HCMV) linked to the neomycin resistance gene. Foci of neomycin-resistant and morphologically transformed cells were isolated and expanded into fourteen RCMV strains. Eight of these strains acquired immortalization, but only one strain (RCMV-21) retained recombined viral sequences integrated in the cellular DNA. RCMV strains were heterogeneous in their morphology, expression of smooth muscle alpha-actin, growth, and mitogenic response to serum and fibroblast growth factor (FGF)-2 and -4. All RCMV strains assayed except RCMV-3 showed DNA synthesis in low serum medium and, with the exception of RCMV-1 cells, all showed a significant mitogenic response to FGF-2 and FGF-4, Maintenance of the transformed phenotype appeared independent of the retention of the transforming viral sequences, which was suggestive of a "hit-and-run" mechanism. These results suggested that morphological transformation by HCMV DNA sequences could enhance the mitogenic response of vascular smooth muscle cells to fibroblast growth factors.
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Dates et versions

hal-02138369 , version 1 (23-05-2019)

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  • HAL Id : hal-02138369 , version 1
  • PUBMED : 9358765

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Alain Legrand, E.P Mayer, S Dalvi, M Nachtigal. Transformation of rabbit vascular smooth muscle cells by human cytomegalovirus morphological transforming region I.. American Journal of Pathology, 1997, 151 (5), pp.1387-95. ⟨hal-02138369⟩

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