| Summary: | Atherosclerosis is an inflammatory disease of the cardiovascular system. Discoidin
domain receptor 1 is a receptor tyrosine kinase that binds collagens. Previous work in our lab has shown that deleting DDR1 in a mouse model results in attenuation of
atherosclerosis, with fewer macrophages in the plaque. The aim of this study was to
determine what changes in macrophage behaviour due to the lack of DDR1 was
attenuating plaque development.
In order to carry out experiments, primary mouse peritoneal macrophages were used.
DDR1-deficient macrophages adhered significantly less to type IV collagen and
fibronectin compared to DDR1-expressing cells. In addition, when plated on type IV
collagen and fibronectin, DDR1-deficient macrophages produced decreased levels of
MCP-1 protein, a cytokine known to be important in plaque development, particularly in leukocyte recruitment to plaque. These results suggest that DDR1 is an important mediator in macrophage adhesion to matrix and macrophage cytokine production
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