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CIRC RES:血管重塑的新机制:分化型但可塑的血管平滑肌细胞增殖促进新生内膜形成

2017-02-23 MedSci MedSci原创

本研究表明这些较低比例但高可塑性VSMCs的广泛增殖可导致血管损伤后和动脉粥样硬化斑块中的VSMCs积聚。靶向治疗这些过度增殖的VSMCs可以有效地减少血管疾病而不影响血管完整性。

血管平滑肌细胞(VSMCs)积聚是动脉粥样硬化和血管损伤的标志。然而,血管疾病时VSMCs的增殖和表型转化的机制尚不清楚,尤其是否所有的VSMCs均有增殖及可塑性,还是个别细胞可转换为多种表型。

近来发表在Circulation research上的一项基础医学研究,旨在评估疾病时的细胞增殖及可塑性是VSMCs的普遍特征或只是细胞亚群的特征。

使用多色谱系标记,我们发现损伤诱导的新生内膜病变和动脉粥样硬化斑块中VSMCs为寡克隆,衍生自少数扩张细胞。谱系追踪也显示个别VSMCs的后代参与了α平滑肌肌动蛋白(αSma)阳性纤维帽和表达Mac3的巨噬细胞样斑块核心细胞。给予VSMC表型标志的共染色进一步鉴定出了aSma + Mac3 +双阳性细胞群,表明这些特异性的斑块细胞是VSMCs来源的。相反,血管损伤后形成的新生内膜中VSMC衍生的细胞通常维持表达VSMCs表型标记物,而Mac3的上调不明显。动脉粥样硬化斑块和损伤诱导的新生内膜中的单色区域不包含表达不同荧光报告蛋白的VSMCs衍生细胞,表明增殖非依赖性VSMCs的迁移不对血管疾病时VSMCs的累积负主要责任。

本研究表明这些较低比例但高可塑性VSMCs的广泛增殖可导致血管损伤后和动脉粥样硬化斑块中的VSMCs积聚。靶向治疗这些过度增殖的VSMCs可以有效地减少血管疾病而不影响血管完整性。

原始出处:
Chappell J, Harman JL, Narasimhan VM,et al.Extensive Proliferation of a Subset of Differentiated, yet Plastic, Medial Vascular Smooth Muscle Cells Contributes to Neointimal Formation in Mouse Injury and Atherosclerosis Models.Circ Res. 2016 Dec 9;119(12):1313-1323. Epub 2016 Sep 28.

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动脉粥样硬化(atherosclerosis,AS)是冠心病、脑梗死、外周血管病的主要原因,是动脉壁上沉积一层包括胆固醇结晶在内的粥样物质,使动脉弹性降低、管腔变窄,常导致心肌梗塞、中风等致命疾病发生。关于近期动脉粥样硬化相关研究重大成果,小M与您分享。【1】Diabetes Care:高级糖基化终末产物、氧化产物和动脉粥样硬化程度相关性分析 近日,糖尿病领域权威杂志Diabetes

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2017年2月15日,国际知名生物化学杂志《Journal of BioLogical Chemistry》在线发表了中国科学院上海生命科学研究院健康科学研究所尹慧勇组的研究论文

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