Endothelial injury releases inflammatory mediators that recruit leukocytes to the area. These cells express growth factors that promote smooth muscle cell migration from the tunica media into the intima. In other cases, pluripotent stem cells migrate from the basement membrane in response to injury. These cells proliferate in the tunica intima and deposit extracellular matrix, leading to thickening of the intima and a reduction in the vascular lumen. Intimal proliferation is an important cause of restenosis, a common complication of endovascular intervention in humans and animal models of vascular disease.
Strains differ in susceptibility to intimal proliferation. C57BL/6, 129SV, SJL/J, C3H, and iNOS-knockout mice are more resistant to the development of intimal proliferation after vascular injury, while FVB/N, C57L/J, and apoE-, RAG2-, eNOS-, and LDLR-knockout mice are highly susceptible to intimal proliferation following vascular injury. Intimal proliferation may also be induced through mechanical injury to the endothelium. The most commonly used procedures to induce arterial injury in mice are carotid artery ligation with cessation of blood flow, and mechanically induced denudation of endothelium in the carotid or femoral arteries. Both procedures result in intimal proliferation after two to three weeks.
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