PubMed · 2662607
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A Maleeva. 1989. [Glucocorticoid secretion in normal and pathologic states].. https://pubmed.ncbi.nlm.nih.gov/2662607/
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The levels of E-selectin mRNA and protein were analyzed in bovine capillary cells treated with or without the angiogenesis inhibitor AGM-1470 (also known as TNP-470). Cells treated with AGM-1470 had a two- to sevenfold (median fivefold) increase in E-selectin mRNA compared with little or no increase in P-selectin, PECAM-1 and VCAM-1 mRNA. E-selectin protein was also significantly increased after exposure to AGM-1470. In contrast, there was no detectable effect on PECAM-1 protein. The increase in E-selectin mRNA and protein was always greater with subconfluent growing cells than with confluent cells. This apparent resistance of confluent endothelial cells to AGM-1470 may be relevant to its specificity in vivo. The fact that the effect of AGM-1470 on E-selectin is relatively selective for subconfluent growing cells may provide a clue as to how AGM-1470 is able to both reversibly inhibit endothelial cell proliferation in vitro and inhibit tumor growth in vivo without apparent effects to quiescent endothelium.
In order to clarify the physiological function of fibroblast growth factor (FGF-2) in the adrenal medulla the regulation of FGF-2 and FGF receptor 1 (FGFR1) was studied in vitro and in vivo in response to glucocorticoids. To assess the effects of glucocorticoids, in vivo extracts of adrenal medulla and adrenal cortex were analyzed by RNase protection assay and Western blot analysis. PC12 cells were chosen as a model system to study the effects of glucocorticoids in vitro. In PC12 cells, dexamethasone (DEX) was found to stimulate dramatically the expression of both FGF-2 mRNA and protein. Western blot analysis revealed that exclusively the 21-kDa FGF-2 isoform was enhanced. In contrast to the FGF-2 mRNA level FGFR1 was not affected by treatment with glucocorticoids. In vivo FGF-2 mRNA level and 21-kDa FGF-2 isoform level are significantly enhanced in the adrenal medulla 24 h after DEX injection. In vivo application of DEX leads to an increase of the medullary and cortical FGFR1 transcript levels. Glucocorticoid effects on FGF-2 expression were not found in adrenal cortex, heart, skeletal muscle, and kidney, respectively, in vivo and in L6 rat myoblasts in vitro. In addition to adrenal medullary cells glucocorticoids elevated the FGF-2 mRNA and protein level also in vivo in the brain and in vitro in immortalized Schwann cells. The present results suggest that the 21-kDa FGF-2 isoform mediates a physiological function specific for neuronal tissue which is modulated by glucocorticoids.
Although the importance of the vascular endothelial growth factor (VEGF)/VEGF tyrosine kinase receptor (VEGFR) system in angiogenesis is well established, very little is known about the regulation of VEGFR expression in vascular endothelial cells. We have cloned partial cDNAs encoding bovine VEGFR-1 (flt) and -2 (flk-1) and used them to study VEGFR expression by bovine microvascular- and large vessel-derived endothelial cells. Both cell lines express flk-1, but not flt. Transforming growth factor beta 1 (TGF-beta 1) reduced the high affinity 125I-VEGF binding capacity of both cell types in a dose-dependent manner, with a 2.0-2.7-fold decrease at 1-10 ng/ml. Cross-linking experiments revealed a decrease in 125I-VEGF binding to a cell surface monomeric protein corresponding to Flk-1 on the basis of its affinity for VEGF, molecular mass (185-190 kDa), and apparent internalization after VEGF binding. Immunoprecipitation and Western blot experiments demonstrated a decrease in Flk-1 protein expression, and TGF-beta 1 reduced flk-1 mRNA levels in a dose-dependent manner. These results imply that TGF-beta 1 is a major regulator of the VEGF/Flk-1 signal transduction pathway in endothelial cells.