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大鼠主动脉中的单核细胞趋化蛋白-1(MCP-1)及其受体CCR2随年龄增长而增加,并改变血管平滑肌细胞功能。

Rat aortic MCP-1 and its receptor CCR2 increase with age and alter vascular smooth muscle cell function.

作者信息

Spinetti Gaia, Wang Mingyi, Monticone Robert, Zhang Jing, Zhao Di, Lakatta Edward G

机构信息

Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA.

出版信息

Arterioscler Thromb Vasc Biol. 2004 Aug;24(8):1397-402. doi: 10.1161/01.ATV.0000134529.65173.08. Epub 2004 Jun 3.

Abstract

OBJECTIVE

With age, rat arterial walls thicken and vascular smooth muscle cells (VSMCs) exhibit enhanced migration and proliferation. Monocyte chemotactic protein-1 (MCP-1) affects these VSMC properties in vitro. Because arterial angiotensin II, which induces MCP-1 expression, increases with age, we hypothesized that aortic MCP-1 and its receptor CCR2 are also upregulated and affect VSMC properties.

METHODS AND RESULTS

Both MCP-1 and CCR2 mRNAs and proteins increased in old (30-month) versus young (8-month) F344xBN rat aortas in vivo. Cellular MCP-1 and CCR2 staining colocalized with that of alpha-smooth muscle actin in the thickened aortas of old rats and were expressed by early-passage VSMCs isolated from old aortas, which, relative to young VSMCs, exhibited increased invasion, and the age difference was abolished by vCCI, an inhibitor of CCR2 signaling. MCP-1 treatment of young VSMCs induced migration and increased their ability to invade a synthetic basement membrane. The MCP-1-dependent VSMC invasiveness was blocked by vCCI. After MCP-1 treatment, migration and invasion capacities of VSMCs from young aortas no longer differed from those of VSMCs isolated from older rats.

CONCLUSIONS

Arterial wall and VSMC MCP-1/CCR2 increase with aging. MCP-1 enhances VSMC migration and invasion, and thus, MCP-1/CCR2 signaling may play a role in age-associated arterial remodeling.

摘要

目的

随着年龄增长,大鼠动脉壁增厚,血管平滑肌细胞(VSMC)迁移和增殖增强。单核细胞趋化蛋白-1(MCP-1)在体外影响这些VSMC特性。由于诱导MCP-1表达的动脉血管紧张素II随年龄增加,我们推测主动脉MCP-1及其受体CCR2也上调并影响VSMC特性。

方法与结果

在体内,老年(30个月)F344xBN大鼠主动脉中MCP-1和CCR2的mRNA及蛋白水平均高于年轻(8个月)大鼠。在老年大鼠增厚的主动脉中,细胞MCP-1和CCR2染色与α-平滑肌肌动蛋白染色共定位,且从老年主动脉分离的早期传代VSMC表达MCP-1和CCR2。相对于年轻VSMC,老年VSMC的侵袭能力增强,而CCR2信号抑制剂vCCI可消除这种年龄差异。用MCP-1处理年轻VSMC可诱导其迁移并增强其侵袭合成基底膜的能力。vCCI可阻断MCP-1依赖的VSMC侵袭性。MCP-1处理后,年轻主动脉VSMC的迁移和侵袭能力与老年大鼠分离的VSMC不再有差异。

结论

动脉壁和VSMC的MCP-1/CCR2随衰老而增加。MCP-1增强VSMC迁移和侵袭,因此,MCP-1/CCR2信号可能在与年龄相关的动脉重塑中起作用。

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