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

      Cardiovascular Pathology
      Animals, Cell Adhesion, drug effects, genetics, Cell Proliferation, Cells, Cultured, Chemotaxis, Collagen Type I, pharmacology, Extracellular Matrix, metabolism, Fibroblasts, cytology, physiology, Gene Deletion, Gene Expression, Gene Silencing, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Mice, Mice, Knockout, Myocytes, Smooth Muscle, Receptor Protein-Tyrosine Kinases, deficiency, Receptors, Mitogen

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          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. Copyright © 2012 Elsevier Inc. All rights reserved.

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