MONOCYTE CHEMOATTRACTANT PROTEIN-1 IN HUMAN ATHEROMATOUS PLAQUES
MONOCYTE CHEMOATTRACTANT PROTEIN-1 IN HUMAN ATHEROMATOUS PLAQUES
复制标题
DOI：
10.1172/jci115411
复制
发表时间：
1991-10-01
影响因子：
15.9
通讯作者：
WILCOX, JN
中科院分区：
文献类型：
--
作者：
NELKEN, NA;COUGHLIN, SR;WILCOX, JN
单核细胞似乎是动脉粥样硬化形成的核心，既作为泡沫细胞的祖细胞，又作为介导内膜增生的生长因子的潜在来源，但刺激单核细胞流入人类动脉粥样硬化的化学信息仍然未知。 单核细胞趋化蛋白-1 (MCP-1) 是最近描述的一种分子，具有强大的单核细胞趋化活性，由培养的单核细胞、血管内皮细胞和平滑肌细胞表达。 为了开始研究 MCP-1 在体内的作用，我们通过原位杂交检查了 10 条正常动脉和 14 条患病人类动脉的 MCP-1 表达。 在人颈动脉内膜切除术标本中计数的 10,768 个细胞中，有 16% 检测到 MCP-1 mRNA，与纤维帽 (8%) 和坏死脂质核心本身 (5%) 相比，在机化血栓 (33%) 和与坏死脂质核心接壤的巨噬细胞丰富区域 (24%) 中表达最高。 根据连续切片的免疫组织化学染色和细胞形态，MCP-1 mRNA 似乎由血管平滑肌细胞 (VSMC)、间充质内膜细胞 (MIC) 和巨噬细胞表达。 相比之下，在正常动脉中很少发现表达 MCP-1 mRNA 的细胞 (< 0.1%)。 这些数据表明 MCP-1 在介导动脉壁单核细胞浸润中具有潜在作用。
Monocytes appear to be central to atherogenesis both as the progenitors of foam cells and as a potential source of growth factors mediating intimal hyperplasia, but the chemical messages which stimulate the influx of monocytes into human atheroma remain unknown. Monocyte chemoattractant protein-1 (MCP-1) is a recently described molecule with powerful monocyte chemotactic activity expressed by monocytes, vascular endothelial cells, and smooth muscle cells in culture. To begin to address the role of MCP-1 in vivo, we examined 10 normal arteries and 14 diseased human arteries for MCP-1 expression by in situ hybridization. MCP-1 mRNA was detected in 16% of 10,768 cells counted in human carotid endarterectomy specimens with highest expression seen in organizing thrombi (33%) and in macrophage rich areas bordering the necrotic lipid core (24%) as compared to the fibrous cap (8%) and the necrotic lipid core itself (5%). Based on immunohistochemical staining of serial sections and on cell morphology, MCP-1 mRNA appeared to be expressed by vascular smooth muscle cells (VSMC), mesenchymal appearing intimal cells (MICs), and macrophages. By contrast, few cells expressing MCP-1 mRNA were found in normal arteries (< 0.1%). These data suggest a potential role for MCP-1 in mediating monocytic infiltration of the artery wall.