Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
Figure 1
Induction of Bcl-2 expression in mice by FGF-2 and Tat. Mice were injected with 1 g of FGF-2 and/or 10 g of Tat, as described in Section 2. After 7 days tissue samples were taken at the injection sites and processed for histological examination by hematoxylin-eosin staining (left panels, 40X magnification). Tissue sections from 12 animals per group were stained with anti-Bcl-2 antibody (right panels, 40X magnification). Induction of KS-like lesions promoted by 1 g FGF-2 (a) was associated with Bcl-2 protein expression (b). The simultaneous inoculation of 1 g FGF-2 and 10 g Tat further increased both lesion development (c) and Bcl-2 expression (d). The inoculation of 10g Tat alone induced only limited histological alterations (e) and no Bcl-2 protein expression (f) at the injection sites. Protein suspension buffer (PBS-0.1% BSA) did not promote lesion development (g), nor Bcl-2 protein expression (h). Arrows point at some representative spindle cells of KS-like lesions.
