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首页> 外文期刊>BioResearch open access. >Differential Effects of IFN-β on the Survival and Growth of Human Vascular Smooth Muscle and Endothelial Cells
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Differential Effects of IFN-β on the Survival and Growth of Human Vascular Smooth Muscle and Endothelial Cells

机译：IFN-β对人血管平滑肌和内皮细胞存活和生长的差异作用

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It has been documented that interferon (IFN)-β is effective against the genesis of atherosclerosis or hyperplastic arterial disease in animal model. The main mechanism of the efficacy was antiproliferative action on the growth of vascular smooth muscle cells (SMC). To understand more about the mechanisms that are responsible for the efficacy, we examined minutely the effects of IFN-β on the apoptosis and growth of vascular SMC and endothelial cells (EC). IFN-β enhanced SMC apoptosis in serum starved medium. Conversely, EC apoptosis induced by serum and growth factor deprivation was inhibited by IFN-β. The induction of SMC apoptosis and anti-apoptotic effect on EC linked to the expression of pro-apoptotic bax mRNA and caspase-3 activities. Anti-apoptotic bcl-2 mRNA was also up-regulated in EC. IFN-β inhibited SMC growth in a dose dependent manner. However, the growth of EC was rather enhanced by a low dose of IFNs. The antiproliferative effect on SMC associated with the activation of p21 and increase of G0/G1 arrested cells. The growth stimulation on EC was considered to link with increase of S and G2/M phase cells. SMC produced IFN-β in response to various stimulants. However, IFN-β was not induced in EC. These suggested that endogenous IFN-β from SMC may act on EC and affect to EC functions. In this study, it was clarified that IFN-β enhances SMC apoptosis and inhibits the EC apoptosis, and stimulates the EC growth. These effects were considered to contribute to a cure against hyperplastic arterial diseases as the mechanisms in the efficacy of IFN-β.
机译：已有文献证明，干扰素（IFN）-β在动物模型中对动脉粥样硬化或增生性动脉疾病的发生有效。功效的主要机制是对血管平滑肌细胞（SMC）生长的抗增殖作用。为了了解更多有关功效的机制，我们仔细检查了IFN-β对血管SMC和内皮细胞（EC）凋亡和生长的影响。 IFN-β增强了血清饥饿培养基中的SMC细胞凋亡。相反，IFN-β抑制了血清和生长因子缺乏引起的EC凋亡。 SMC凋亡的诱导和对EC的抗凋亡作用与促凋亡bax mRNA和caspase-3活性的表达有关。 EC中的抗凋亡bcl-2 mRNA也被上调。 IFN-β以剂量依赖性方式抑制SMC生长。但是，低剂量的IFN可以促进EC的生长。对SMC的抗增殖作用与p21的激活和G0 / G1被阻滞细胞的增加有关。认为EC上的生长刺激与S和G2 / M期细胞的增加有关。 SMC响应各种刺激物产生IFN-β。然而，在EC中未诱导IFN-β。这些提示来自SMC的内源性IFN-β可能作用于EC并影响EC功能。在该研究中，明确了IFN-β增强SMC凋亡并抑制EC凋亡，并刺激EC生长。这些作用被认为有助于治疗增生性动脉疾病，这是IFN-β功效的机制。

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