[Roles of monocyte chemoattractant protein-1, RANTES and Fractalkine on promoting vulnerability of atherosclerotic plaques]

Zhonghua Xin Xue Guan Bing Za Zhi. 2011 Sep;39(9):797-801.
[Article in Chinese]

Abstract

Objective: To elucidate the roles of monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) on the vulnerability of atherosclerotic plaques in patients with stable (SAP) and unstable angina pectoris (UAP).

Methods: Patients with SAP (n = 50) and UAP (n = 50) underwent coronary angiography (CAG) and intravenous ultrasound (IVUS) were included in the study. Monocyte chemotaxis was assayed by the transwell chamber. Concentrations of hs-CRP, MCP-1, RANTES and Fractalkine were measured by Enzyme-linked-immunosorbent assay (ELISA). mRNA expression of MCP-1, RANTES and Fractalkine in the monocytes was detected by RT-PCR.

Results: IVUS evidenced soft lipid plaques in 48% UAP patients and in 16% SAP patients (P < 0.05). SAP patients had mainly fibrous and mixed plaques. Plaque burden and vascular remodeling index were significantly higher in UAP patients than in SAP patients (P < 0.01). The averaged number of migrated monocytes in the UAP patients were higher than that in patients with SAP (P < 0.01). Concentration of hs-CRP, MCP-1, RANTES and Fractalkine were significantly higher in UAP patients than those of SAP patients (P < 0.05 or P < 0.01). mRNA expression of MCP-1, RANTES and Fractalkine in patients with UAP was significantly higher than those of SAP patients (P < 0.05).

Conclusion: Upregulated monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) might promote coronary plaque vulnerability in UAP patients.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angina Pectoris / metabolism*
  • Angina Pectoris / pathology
  • Angina, Unstable / metabolism*
  • Angina, Unstable / pathology
  • Chemokine CCL2 / metabolism*
  • Chemokine CCL5 / metabolism*
  • Chemokine CX3CL1 / metabolism*
  • Coronary Angiography
  • Female
  • Humans
  • Male
  • Middle Aged
  • Plaque, Atherosclerotic / pathology*
  • RNA, Messenger / genetics

Substances

  • CCL2 protein, human
  • CCL5 protein, human
  • CX3CL1 protein, human
  • Chemokine CCL2
  • Chemokine CCL5
  • Chemokine CX3CL1
  • RNA, Messenger