白介素37促进血管生成的分子机制研究
首发时间:2017-05-17
摘要:白介素37(IL-37)是IL-1家族成员之一,具有抗炎作用,同时IL-37在多种血管增生相关疾病中上调。我们前期研究中发现,IL-37具有显著的促进内皮细胞活化和病理性血管生成的功能,且可与具有促血管生成功能的TGF-β受体ALK1结合。然而IL-37的促血管生成效应背后的机制不甚了解。基于我们已有的研究成果,我们采用受体竞争结合、免疫共沉淀以及体外结合实验等模型,深入研究IL-37促进血管生成的分子机制。我们发现TGF-β与IL-37相互作用,并且有效地增强IL-37与ALK1受体复合物的结合亲和力,从而允许IL-37通过ALK1信号通路激活促血管生成反应。
关键词: 白介素37 转化生长因子-β 激活素受体样激酶1, 血管生成
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Interleukin 37 promotes angiogenesis through TGF-β signaling
Abstract:Interleukin -37 (IL-37) is an anti-inflammatory cytokine of the IL-1 family and is upregulated in many angiogenesis related diseases. Our previous study found that IL-37 potently promotes endothelial cell activation and pathological angiogenesis. We find that IL-37 binds with ALK-1, a receptor of TGF-β which promotes angiogenesis. However, the mechanisms underlying the pro-angiogenic effects of IL-37 are poorly understood. Based on our previous studies, we investigated the molecular mechanism by which IL-37 promotes angiogenesis using models of receptor binding assay and Co-IP. We found that TGF-β interacts with IL-37 and effectively enhance the binding affinity of IL-37 to the ALK-1 receptor complex, thereby allowing IL-37 to activate the angiogenic response.
Keywords: IL-37, TGF-β, ALK-1, Angiogenesis
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No.4733575119983214****
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