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Pro-osteogenic phenotype of human aortic valve interstitial cells is associated with higher levels of Toll-like receptors 2 and 4 and enhanced expression of bone morphogenetic protein 2.人主动脉瓣间质细胞的促骨生成表型与Toll样受体2和4的较高水平以及骨形态发生蛋白2的表达增强有关。
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Altered shear stress stimulates upregulation of endothelial VCAM-1 and ICAM-1 in a BMP-4- and TGF-beta1-dependent pathway.改变的剪切应力通过骨形态发生蛋白4（BMP-4）和转化生长因子β1（TGF-β1）依赖的途径刺激内皮细胞血管细胞黏附分子1（VCAM-1）和细胞间黏附分子1（ICAM-1）的上调。
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High-density lipoproteins affect endothelial BMP-signaling by modulating expression of the activin-like kinase receptor 1 and 2.高密度脂蛋白通过调节激活素样激酶受体1和2的表达来影响内皮骨形态发生蛋白信号传导。
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Bone morphogenetic proteins 2 and 4 are selectively expressed by late outgrowth endothelial progenitor cells and promote neoangiogenesis.骨形态发生蛋白2和4由晚期生长的内皮祖细胞选择性表达，并促进新生血管形成。
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BMPER is an endothelial cell regulator and controls bone morphogenetic protein-4-dependent angiogenesis.BMPER是一种内皮细胞调节剂，可控制骨形态发生蛋白-4依赖性血管生成。
Circ Res. 2008 Oct 10;103(8):804-12. doi: 10.1161/CIRCRESAHA.108.178434. Epub 2008 Sep 11.
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Cardiac commitment of primate embryonic stem cells.灵长类胚胎干细胞向心脏的定向分化
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7
SM22alpha-targeted deletion of bone morphogenetic protein receptor 1A in mice impairs cardiac and vascular development, and influences organogenesis.在小鼠中靶向删除骨形态发生蛋白受体1A的SM22α会损害心脏和血管发育，并影响器官发生。
Development. 2008 Sep;135(17):2981-91. doi: 10.1242/dev.017863. Epub 2008 Jul 30.
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Oxidative stress impairs endothelial progenitor cell function.氧化应激会损害内皮祖细胞的功能。
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血流动力、血管氧化应激与 BMP-2/4 表达的调控。

Hemodynamic forces, vascular oxidative stress, and regulation of BMP-2/4 expression.

机构信息

Department of Physiology, New York Medical College, Valhalla, New York, USA.

出版信息

Antioxid Redox Signal. 2009 Jul;11(7):1683-97. doi: 10.1089/ars.2008.2401.

DOI:10.1089/ars.2008.2401
PMID:19320562
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2842584/
Abstract

Changes in the hemodynamic environment (e.g., hypertension, disturbed-flow conditions) are known to promote atherogenesis by inducing proinflammatory phenotypic alterations in endothelial and smooth muscle cells; however, the mechanisms underlying mechanosensitive induction of inflammatory gene expression are not completely understood. Bone morphogenetic protein-2 and -4 (BMP-2/4) are TGF-beta superfamily cytokines that are expressed by both endothelial and smooth muscle cells and regulate a number of cellular processes involved in atherogenesis, including vascular calcification and endothelial activation. This review considers how hemodynamic forces regulate BMP-2/4 expression and explores the role of mechanosensitive generation of reactive oxygen species by NAD(P)H oxidases in the control of BMP signaling.

摘要

血流动力学环境的变化（例如高血压、血流紊乱等）已知可通过诱导内皮细胞和平滑肌细胞的促炎表型改变来促进动脉粥样硬化形成；然而，机械敏感诱导炎症基因表达的机制尚不完全清楚。骨形态发生蛋白 2 和 4（BMP-2/4）是 TGF-β超家族细胞因子，内皮细胞和平滑肌细胞均可表达，并调节动脉粥样硬化形成过程中涉及的许多细胞过程，包括血管钙化和内皮细胞激活。本综述考虑了血流动力学如何调节 BMP-2/4 的表达，并探讨了 NAD(P)H 氧化酶产生的机械敏感活性氧在控制 BMP 信号中的作用。