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Previous studies have demonstrated that expression of galectin-3, a member of family of beta-galactosidebinding animal lectin, is associated with pathological conditions including cancer, atherosclerosis, and viral infection. An increase of this lectin has been observed after infection by Kirsten murine sarcoma, human T lymphotropic virus-1 (HTLV-1), and human immunodeficiency virus-1 (HIV-1). Viral transactivation protein Tax of HTLV-1 mediates the increase in the lectin. In case of HIV-1, there are evidences that Tat would be related with increase in galectin-3. We investigated whether Tat directly induced galectin-3 expression in cells. We found that HIV-1 tat gene activated galectin-3 promoter in RAW264.7 cells. To demonstrate direct induction of galectin-3 by HIV-1 tat, we transfected the tat into a rabbit smooth muscle cell line (Rb1) and obtained Rb1TatCl-2, a clone of cell stably transfected with tat gene. The Rb1TatCl-2 cells exhibited activation of LTR promoter and up-regulation of galectin-3 transcript as well as protein. Our results indicate that HIV-1 tat alone is sufficient to induce the expression of galectin-3. The Rb1TatCl-2 cells could be valuable for study of the effect of HIV-1 tat on expression of cellular genes.
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