Abstract
Background: Angiotensin 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. Methods: Six-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. Results: Ang 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. Conclusion: These 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.
Original language | English (US) |
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Pages (from-to) | 231-236 |
Number of pages | 6 |
Journal | Cardiovascular Pathology |
Volume | 16 |
Issue number | 4 |
DOIs | |
State | Published - Jul 2007 |
Keywords
- Angiotensin II
- Carotid artery ligation
- MCP-1
- MIP-1α
- Proliferation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pathology and Forensic Medicine