Abstract | BACKGROUND: METHODS: Six-month-old male C57BL/6-, MCP-1-, or MIP-1alpha-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-1alpha 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-1alpha deficiency failed to affect intimal hyperplasia in vascular remodeling. CONCLUSION: These results indicate that MCP-1 or MIP-1alpha 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.
|
Authors | Le-Ning Zhang, Valdeci da Cunha, Baby Martin-McNulty, John Rutledge, Ronald Vergona, Mark E Sullivan, Yi-Xin Jim Wang |
Journal | Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
(Cardiovasc Pathol)
2007 Jul-Aug
Vol. 16
Issue 4
Pg. 231-6
ISSN: 1054-8807 [Print] United States |
PMID | 17637431
(Publication Type: Journal Article)
|
Chemical References |
- Ccl2 protein, mouse
- Chemokine CCL2
- Chemokine CCL3
- Chemokine CCL4
- Macrophage Inflammatory Proteins
- Angiotensin II
|
Topics |
- Angiotensin II
(metabolism)
- Animals
- Carotid Arteries
(metabolism, pathology)
- Carotid Artery Injuries
(metabolism, pathology)
- Chemokine CCL2
(metabolism)
- Chemokine CCL3
- Chemokine CCL4
- Hyperplasia
- Immunohistochemistry
- Ligation
- Macrophage Inflammatory Proteins
(metabolism)
- Male
- Mice
- Mice, Inbred C57BL
- Tunica Intima
(metabolism, pathology)
|