J Stroke.  2018 Jan;20(1):80-91. 10.5853/jos.2017.02390.

Differences between the Molecular Mechanisms Underlying Ruptured and Non-Ruptured Carotid Plaques, and the Significance of ABCA1

Affiliations
  • 1Department of Neurology, Kyung Hee University School of Medicine, Seoul, Korea. dichang@khmc.or.kr
  • 2Department of Neurology, Hanyang University College of Medicine, Seoul, Korea. ksh213@hanyang.ac.kr
  • 3Department of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul, Korea.
  • 4Department of Thoracic and Cardiovascular Surgery, Kyung Hee University School of Medicine, Seoul, Korea.

Abstract

BACKGROUND AND PURPOSE
Carotid plaques are a strong risk factor for ischemic stroke, and plaque rupture poses an even higher risk. Although many studies have investigated the pathogenic mechanisms of carotid plaque formation, few have studied the differences in molecular mechanisms underlying the rupture and non-rupture of carotid plaques. In addition, since early diagnosis and treatment of carotid plaque rupture are critical for the prevention of ischemic stroke, many studies have sought to identify the important target molecules involved in the rupture. However, a target molecule critical in symptomatic ruptured plaques is yet to be identified.
METHODS
A total of 79 carotid plaques were consecutively collected, and microscopically divided into ruptured and non-ruptured groups. Quantitative polymerase chain reaction array, proteomics, and immunohistochemistry were performed to compare the differences in molecular mechanisms between ruptured and non-ruptured plaques. Enzyme-linked immunosorbent assay was used to measure the differences in ATP-binding cassette subfamily A member 1 (ABCA1) levels in the serum.
RESULTS
The expression of several mRNAs and proteins, including ABCA1, was higher in ruptured plaques than non-ruptured plaques. In contrast, the expression of other proteins, including β-actin, was lower in ruptured plaques than non-ruptured plaques. The increased expression of ABCA1 was consistent across several experiments, ABCA1 was positive only in the serum of patients with symptomatic ruptured plaques.
CONCLUSIONS
This study introduces a plausible molecular mechanism underlying carotid plaque rupture, suggesting that ABCA1 plays a role in symptomatic rupture. Further study of ABCA1 is needed to confirm this hypothesis.

Keyword

Carotid arteries; Plaque; ABCA1; Rupture; Proteomics; Biomarkers

MeSH Terms

Biomarkers
Carotid Arteries
Early Diagnosis
Enzyme-Linked Immunosorbent Assay
Humans
Immunohistochemistry
Polymerase Chain Reaction
Proteomics
Risk Factors
RNA, Messenger
Rupture
Stroke
Biomarkers
RNA, Messenger
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