Abstract
Our previous studies show that growth hormone overexpression (GHo) upregulates the expression of the IGF-1R and IGF-2R resulting in the protection of the EL4 lymphoma cell line from apoptosis. In this study, we report that GHo also increases TGF-β1 protein expression measured by luciferase promoter assay, Western analysis, and ELISA. Further, the data show that antibody to TGF-βR2 decreases TGF-β1 promoter activity to the level of vector alone control cells. GHo cells treated with 125I-rh-latent TGF-β1 showed increased activation of latent TGF-β1 as measured by an increase in the active 24 kDa, TGF-β1 compared to vector alone control cells. The ability of endogenous GH to increase TGF-β1 expression is blocked in EL4 cells by antisense but not sense oligodeoxynucleotides or in cells cultured with antibody to growth hormone (GH). The data suggest that endogenous GH may protect from apoptosis through the IGF-1R receptor while limiting cellular growth through increased expression and activation of TGF-β1.
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