Indirect angiogenic cytokines upregulate VEGF and bFGF gene expression in vascular smooth muscle cells, whereas hypoxia upregulates VEGF expression only.
Indirect angiogenic cytokines upregulate VEGF and bFGF gene expression in vascular smooth muscle cells, whereas hypoxia upregulates VEGF expression only.
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DOI：
10.1097/00006982-199515020-00024
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发表时间：
1994
期刊：
影响因子：
37.8
通讯作者：
E. Brogi;Tian-gen Wu;A. Namiki;J. Isner
中科院分区：
文献类型：
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作者：
E. Brogi;Tian-gen Wu;A. Namiki;J. Isner
缺氧和间接血管生成因子可通过诱导内皮细胞有丝分裂原刺激血管生成。为了评估这一假设，我们研究了低氧张力或已知促进体内新血管形成的细胞因子是否可以调节人血管平滑肌细胞（SMC）中血管内皮生长因子（VEGF）或碱性成纤维细胞生长因子（bFGF）的表达。方法和结果SMC分别用血小板衍生生长因子BB（PDGF-BB）或转化生长因子β 1（TGF-β 1）处理，或在无血清培养基中暴露于低氧张力。北方分析检测到低基础水平的VEGF和bFGF mRNA的提取物未刺激的SMC。然而，在给予PDGF-BB（10或20 ng/mL）或TGF-β 1（0.1至10 ng/mL）后，VEGF和bFGF转录物均增加。缺氧是一个有力的刺激VEGF基因表达，但没有明显的影响bFGF稳态mRNA水平。结论某些间接促血管生成的细胞因子，如PDGF-BB或TGF-β 1，可能通过诱导位于内皮细胞附近的细胞中bFGF和VEGF基因表达而起作用。缺氧是VEGF基因表达的有效刺激物，但在相同的实验条件下不能调节bFGF。
BACKGROUND Hypoxia and indirect angiogenic factors may stimulate angiogenesis via induction of endothelial cell mitogen(s). To evaluate this hypothesis, we investigated whether low oxygen tension or cytokines known to promote neovascularization in vivo could modulate the expression of either vascular endothelial growth factor (VEGF) or basic fibroblast growth factor (bFGF) in human vascular smooth muscle cells (SMCs). METHODS AND RESULTS SMCs were treated with platelet-derived growth factor BB (PDGF-BB) or transforming growth factor-beta 1 (TGF-beta 1) or exposed to low oxygen tension in serum-free medium. Northern analysis detected low basal levels of VEGF and bFGF mRNA in extracts of unstimulated SMCs. However, both VEGF and bFGF transcripts increased after administration of PDGF-BB (10 or 20 ng/mL) or TGF-beta 1 (0.1 to 10 ng/mL). Hypoxia was a potent stimulus for VEGF gene expression but had no apparent effect on bFGF steady-state mRNA levels. CONCLUSIONS These results indicate that certain indirect angiogenic cytokines, such as PDGF-BB or TGF-beta 1, may act via induction of bFGF and VEGF gene expression in cells resident near endothelial cells in vivo. Hypoxia constitutes a potent stimulus for VEGF gene expresion but does not regulate bFGF under the same experimental conditions.