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

Le Ning Zhang, Valdeci da Cunha, Baby Martin-McNulty, John C Rutledge, Ronald Vergona, Mark E. Sullivan, Yi Xin (Jim) Wang

Research output: Contribution to journalArticle

3 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)231-236
Number of pages6
JournalCardiovascular Pathology
Volume16
Issue number4
DOIs
StatePublished - Jul 2007

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Tunica Intima
Macrophage Inflammatory Proteins
Protein Deficiency
Chemokine CCL2
Carotid Arteries
Angiotensin II
Hyperplasia
Ligation
Infusion Pumps
Adventitia
Common Carotid Artery
Inbred C57BL Mouse
Vascular Diseases
Chemokines
Up-Regulation

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 journalArticle

Zhang, Le Ning ; da Cunha, Valdeci ; Martin-McNulty, Baby ; Rutledge, John C ; Vergona, Ronald ; Sullivan, Mark E. ; Wang, Yi Xin (Jim). / Monocyte chemoattractant protein-1 or macrophage inflammatory protein-1α deficiency does not affect angiotensin II-induced intimal hyperplasia in carotid artery ligation model. In: Cardiovascular Pathology. 2007 ; Vol. 16, No. 4. pp. 231-236.
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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.

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