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Discoidin domain receptor 2 缺失并不影响平滑肌细胞对 I 型胶原的黏附、迁移和增殖反应。

Deletion of discoidin domain receptor 2 does not affect smooth muscle cell adhesion, migration, or proliferation in response to type I collagen.

机构信息

Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.

出版信息

Cardiovasc Pathol. 2012 May-Jun;21(3):214-8. doi: 10.1016/j.carpath.2011.07.006. Epub 2011 Aug 23.

DOI:10.1016/j.carpath.2011.07.006
PMID:21865059
Abstract

Collagen receptors expressed on vascular smooth muscle cells include the discoidin domain receptors (DDR1 and DDR2). DDR1 is known to play important roles in mediating smooth muscle cell responses to vascular injury, including neointimal hyperplasia, but much less is known about the function of DDR2. In this study, we harvested smooth muscle cells from DDR2 wild-type and knockout mice and studied the cells using in vitro models of migration and growth. There were no significant differences in the ability of Ddr2(+/+) or Ddr2(-/-) smooth muscle cells to attach to, migrate, or proliferate on type I collagen. Furthermore, neither matrix metalloproteinase (MMP) 2 nor MMP-9 activity nor type I collagen expression was different between the cell types. We conclude that in vitro, endogenous DDR2 is not required for smooth muscle cell hyperplastic responses to collagen.

摘要

血管平滑肌细胞表达的胶原蛋白受体包括盘状结构域受体(DDR1 和 DDR2)。已知 DDR1 在介导血管损伤后平滑肌细胞的反应中发挥重要作用,包括新生内膜增生,但 DDR2 的功能知之甚少。在这项研究中,我们从 DDR2 野生型和敲除小鼠中分离出平滑肌细胞,并使用体外迁移和生长模型研究这些细胞。Ddr2(+/+)或 Ddr2(-/-)平滑肌细胞在 I 型胶原上附着、迁移或增殖的能力没有显著差异。此外,两种细胞类型的基质金属蛋白酶(MMP)2 和 MMP-9 活性或 I 型胶原表达也没有差异。我们的结论是,在体外,内源性 DDR2 对于平滑肌细胞对胶原蛋白的增生反应不是必需的。

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