Monocyte chemoattractant protein-1 or macrophage inflammatory protein-1α deficiency does not affect angiotensin II-induced intimal hyperplasia in carotid artery ligation model

BackgroundAngiotensin II (Ang II) promotes atherosclerotic vascular diseases, in which proinflammatory and proliferative effects play a major pathogenic role. Ang II up-regulates chemokines, such as monocyte chemoattractant protein (MCP)-1 and macrophage inflammatory protein (MIP)-1α, which are important pro-inflammatory factors mediating infiltration of inflammatory cells into atherosclerotic lesion. The aim of the present study was to determine whether the presence of MCP-1 or MIP-1α is essential in Ang II-induced intimal hyperplasia in the carotid artery ligation model.MethodsSix-month-old male C57BL/6-, MCP-1-, or MIP-1α-deficient mice underwent ligation of the common left carotid artery and were randomly assigned to receive either vehicle or Ang II (1.4 mg kg−1 day−1) via a subcutaneously implanted osmotic infusion pump (model 2004, Alzet) for 4 weeks.ResultsAng II not only increased MCP-1 and MIP-1α production but also enhanced neo-intimal formation, media thickness, and adventitia development in the ligated carotid arteries in C57BL/6 mice. However, MCP-1 or MIP-1α deficiency failed to affect intimal hyperplasia in vascular remodeling.ConclusionThese results indicate that MCP-1 or MIP-1α may not be essential in mediating the proliferative effects of Ang II, a major pathological changes in intimal hyperplasia in the carotid artery ligation model.