4.4 Article

Different Distribution of Pentraxin 3 and C-Reactive Protein in Coronary Atherosclerotic Plaques

Journal

JOURNAL OF ATHEROSCLEROSIS AND THROMBOSIS
Volume 19, Issue 9, Pages 837-845

Publisher

JAPAN ATHEROSCLEROSIS SOC
DOI: 10.5551/jat.12526

Keywords

Pentraxin 3 (PTX3); C-reactive protein (CRP); Coronary artery disease; Intraplaque hemorrhage; Macrophages

Funding

  1. Ministry of Education, Science, Sports and Culture of Japan [20590344, 23390084]
  2. Grants-in-Aid for Scientific Research [23390084, 20590344] Funding Source: KAKEN

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Aim: To understand the differences between histopathological characteristics related to PTX3 (pentraxin 3) and CRP (C-reactive protein) in coronary atherosclerotic plaques. Methods and Results: To assess the localization of PTX3 and CRP in coronary plaque, immunohistochemistry was performed using 157 coronary artery specimens from 45 autopsied cases. Overall, immunoreactivity to CRP was more intense than that to PTX3 in lipid rich plaque; however, PTX3 was notably abundant in areas of intraplaque hemorrhage, in which CRP was quite sparse. On quantitative analysis, complicated plaques showed more immunopositive area of PTX3 than fibroatheroma, but with CRP, this trend disappeared. In addition, we examined the phenotype of macrophages in PTX3- and CRP-rich areas using CD163 staining (M2 macrophages). Consequently, these areas were differently characterized by the accumulation of macrophages with high and low magnitude of CD163 positivity, respectively. Next, we immunohistochemically investigated relationships among PTX3, CRP, histological components and clinical presentation in 73 coronary atherectomy specimens obtained from 35 and 38 patients with unstable (UAP) and stable angina pectoris (SAP), respectively. Both PTX3 and CRP were more intense in culprit plaques from patients with UAP than with SAP, and they significantly correlated with CD68 (pan macrophage)-positive areas; however, there was no correlation between PTX3 and CRP. Conclusion: Although PTX3 and CRP were more enhanced in unstable than in stable coronary plaques, their distribution distinctly differed, suggesting that they play distinct biological roles in unstable plaques.

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