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) |
|---|---|
| Pages (from-to) | 231-236 |
| Number of pages | 6 |
| Journal | Cardiovascular Pathology |
| Volume | 16 |
| Issue number | 4 |
| DOIs | |
| State | Published - Jul 2007 |
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Keywords
- Angiotensin II
- Carotid artery ligation
- MCP-1
- MIP-1α
- Proliferation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pathology and Forensic Medicine
Cite this
Monocyte chemoattractant protein-1 or macrophage inflammatory protein-1α deficiency does not affect angiotensin II-induced intimal hyperplasia in carotid artery ligation model. / Zhang, Le Ning; da Cunha, Valdeci; Martin-McNulty, Baby; Rutledge, John C; Vergona, Ronald; Sullivan, Mark E.; Wang, Yi Xin (Jim).
In: Cardiovascular Pathology, Vol. 16, No. 4, 07.2007, p. 231-236.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Monocyte chemoattractant protein-1 or macrophage inflammatory protein-1α deficiency does not affect angiotensin II-induced intimal hyperplasia in carotid artery ligation model
AU - Zhang, Le Ning
AU - da Cunha, Valdeci
AU - Martin-McNulty, Baby
AU - Rutledge, John C
AU - Vergona, Ronald
AU - Sullivan, Mark E.
AU - Wang, Yi Xin (Jim)
PY - 2007/7
Y1 - 2007/7
N2 - 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.
AB - 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.
KW - Angiotensin II
KW - Carotid artery ligation
KW - MCP-1
KW - MIP-1α
KW - Proliferation
UR - http://www.scopus.com/inward/record.url?scp=34447264052&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34447264052&partnerID=8YFLogxK
U2 - 10.1016/j.carpath.2007.01.006
DO - 10.1016/j.carpath.2007.01.006
M3 - Article
C2 - 17637431
AN - SCOPUS:34447264052
VL - 16
SP - 231
EP - 236
JO - Cardiovascular Pathology
JF - Cardiovascular Pathology
SN - 1054-8807
IS - 4
ER -