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膜联蛋白A3是一种潜在的血管生成介质。

Annexin A3 is a potential angiogenic mediator.

作者信息

Park Jae Eun, Lee Do Hee, Lee Jung A, Park Sung Goo, Kim Nam-Soon, Park Byoung Chul, Cho Sayeon

机构信息

Systemic Proteomics Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejon 305-333, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2005 Dec 2;337(4):1283-7. doi: 10.1016/j.bbrc.2005.10.004. Epub 2005 Oct 10.

DOI:10.1016/j.bbrc.2005.10.004
PMID:16236264
Abstract

Angiogenesis is a complex process that is regulated by a variety of angiogenic activators and inhibitors. Disruption of the balanced angiogenesis leads to the progress of diseases such as tumor growth, rheumatoid arthritis, and various blood vessel-related disorders. Even though a number of proteins involved in angiogenesis have been identified so far, more protein factors remain to be identified due to complexity of the process. Here we report that annexin A3 (ANXA3) induces migration and tube formation of human umbilical vein endothelial cells. High level of vascular endothelial growth factor (VEGF), a prominent angiogenic factor, is also detected in conditioned medium obtained from cells transfected with ANXA3 expression plasmid. Reporter assays show that ANXA3 enhances hypoxia-inducible factor-1 (HIF-1) transactivation activity. Taken together, our results suggest that ANXA3 is a novel angiogenic factor that induces VEGF production through the HIF-1 pathway.

摘要

血管生成是一个复杂的过程,受到多种血管生成激活剂和抑制剂的调节。血管生成平衡的破坏会导致诸如肿瘤生长、类风湿性关节炎和各种血管相关疾病的进展。尽管到目前为止已经鉴定出许多参与血管生成的蛋白质,但由于该过程的复杂性,仍有更多的蛋白质因子有待鉴定。在此我们报告,膜联蛋白A3(ANXA3)可诱导人脐静脉内皮细胞迁移和形成管腔结构。在转染了ANXA3表达质粒的细胞所获得的条件培养基中也检测到高水平的血管内皮生长因子(VEGF),这是一种重要的血管生成因子。报告基因检测表明,ANXA3增强缺氧诱导因子-1(HIF-1)的反式激活活性。综上所述,我们的结果表明ANXA3是一种新型血管生成因子,它通过HIF-1途径诱导VEGF产生。

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Annexin A3 is a potential angiogenic mediator.膜联蛋白A3是一种潜在的血管生成介质。
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Angiogenic effects of human multipotent stromal cell conditioned medium activate the PI3K-Akt pathway in hypoxic endothelial cells to inhibit apoptosis, increase survival, and stimulate angiogenesis.人多能基质细胞条件培养基的血管生成作用可激活缺氧内皮细胞中的PI3K-Akt信号通路,从而抑制细胞凋亡、提高细胞存活率并刺激血管生成。
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Hypoxia-inducible factor-1alpha and -2alpha additively promote endothelial vasculogenic properties.缺氧诱导因子-1α和-2α协同促进内皮血管生成特性。
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Activation of fractalkine/CX3CR1 by vascular endothelial cells induces angiogenesis through VEGF-A/KDR and reverses hindlimb ischaemia.血管内皮细胞对趋化因子/ CX3CR1的激活通过血管内皮生长因子-A/激酶插入域受体诱导血管生成,并逆转后肢缺血。
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