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首页> 外文期刊>Journal of Cellular Physiology >Induction of angiogenesis by smooth muscle cell-derived factor: possible role in neovascularization in atherosclerotic plaque.
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Induction of angiogenesis by smooth muscle cell-derived factor: possible role in neovascularization in atherosclerotic plaque.

机译:由平滑肌诱导血管生成细胞衍生因素:可能的作用新血管形成动脉粥样硬化斑块。

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The development of atherosclerotic plaque is associated with neovascularization in the thickened intima and media of vascular walls. Neovascularization may have a role in the progression of atherosclerotic plaque as well as in the development of intraplaque hemorrhage. However, the mechanism and stimulus for neovascularization in atherosclerotic plaque are unknown. We postulated that smooth muscle cells (SMCs), a major cellular component in the vascular wall, might contribute to the induction of neovascularization in atherosclerotic plaque through the secretion of an angiogenic factor. We observed that endothelial cells (ECs) cultured on collagen gel with SMC-conditioned medium became spindle shaped, invaded the underlying collagen gel, and organized a capillary-like branching cord structure in the collagen gel. The conditioned medium also stimulated EC proliferation and increased the EC-associated plasminogen activator activity. The angiogenic factor in SMC-conditioned medium was retained in a heparin-Sepharose column and eluted with 0.9 M NaCl. Neutralizing anti-vascular endothelial growth factor (VEGF) antibody attenuated the angiogenic activity in the conditioned medium, including the induction of morphologic changes in ECs, mitogenic activity, and increased plasminogen activator activity associated with ECs. Immunoblotting analysis confirmed the secretion of VEGF from SMCs. These observations indicate that SMC may be responsible for the neovascularization in atherosclerotic plaque through the secretion of VEGF.
机译:动脉粥样硬化斑块的发展相关的新血管形成血管壁内膜增厚和媒体。新血管形成可能有作用动脉粥样硬化斑块的进展发展的intraplaque出血。然而,机制和刺激新血管形成动脉粥样硬化斑块未知的。(smc)的主要细胞成分血管壁,可能导致感应新血管形成的动脉粥样硬化斑块通过血管生成因子的分泌。观察到内皮细胞(ECs)培养胶原蛋白凝胶与SMC-conditioned介质纺锤形,入侵底层胶原蛋白凝胶,组织了一个capillary-like分支索结构的胶原蛋白凝胶。条件培养基也刺激了电子商务核扩散和增加了EC-associated纤溶酶原激活物的活动。因素SMC-conditioned中被保留heparin-Sepharose列和筛选了0.9生理盐水。生长因子(VEGF)抗体减弱血管生成条件培养液的活动,包括感应的形态学变化ECs,促有丝分裂的活动,增加了纤溶酶原激活物活动联系在一起ECs。从smc VEGF的分泌。表明,SMC可能负责新血管形成的动脉粥样硬化斑块通过VEGF的分泌。

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