Detection of a High Ratio of Soluble to Membrane‐Bound LOX‐1 in Aspirated Coronary Thrombi From Patients With ST‐Segment–Elevation Myocardial Infarction

Author:

Lee An‐Sheng12,Wang Yu‐Chen2345,Chang Shih‐Sheng5,Lo Ping‐Hang5,Chang Chia‐Ming2,Lu Jonathan67,Burns Alan R.8,Chen Chu‐Huang69,Kakino Akemi1011,Sawamura Tatsuya1011,Chang Kuan‐Cheng2512

Affiliation:

1. Department of Medicine Mackay Medical College New Taipei City Taiwan

2. Cardiovascular Research Laboratory China Medical University Hospital Taichung Taiwan

3. Division of Cardiovascular Medicine Asia University Hospital Taichung Taiwan

4. Department of Biotechnology Asia University Taichung Taiwan

5. Division of Cardiovascular Medicine China Medical University Hospital Taichung Taiwan

6. Vascular and Medicinal Research Texas Heart Institute Houston TX

7. InVitro Cell Research LLC Englewood NJ

8. College of Optometry University of Houston Houston TX

9. New York Heart Research Foundation Mineola NY

10. Department of Life Innovation Institute for Biomedical Sciences Shinshu University Matsumoto Japan

11. Department of Molecular Pathophysiology Shinshu University School of Medicine Matsumoto Japan

12. Graduate Institute of Biomedical Sciences China Medical University Taichung Taiwan

Abstract

Background The circulating level of soluble lectin‐like oxidized low‐density lipoprotein receptor‐1 ( sLOX ‐1) is a valuable biomarker of acute myocardial infarction ( AMI ). The most electronegative low‐density lipoprotein, L5, signals through LOX ‐1 to trigger atherogenesis. We examined the characteristics of LOX ‐1 and the role of L5 in aspirated coronary thrombi of AMI patients. Methods and Results Intracoronary thrombi were aspirated by performing interventional thrombosuction in patients with ST ‐segment–elevation myocardial infarction ( STEMI ; n=32) or non–ST‐segment–elevation myocardial infarction (n=12). LOX ‐1 level and the ratio of sLOX ‐1 to membrane‐bound LOX ‐1 were higher in thrombi of STEMI patients than in those of non–ST‐segment–elevation myocardial infarction patients. In all aspirated thrombi, LOX ‐1 colocalized with apoB100. When we explored the role of L5 in AMI , deconvolution microscopy showed that particles of L5 but not L1 (the least electronegative low‐density lipoprotein) quickly formed aggregates prone to retention in thrombi. Treating human monocytic THP ‐1 cells with L5 or L1 showed that L5 induced cellular adhesion and promoted the differentiation of monocytes into macrophages in a dose‐dependent manner. In a second cohort of AMI patients, the L5 percentage and plasma concentration of sLOX ‐1 were higher in STEMI patients (n=33) than in non–ST‐segment–elevation myocardial infarction patients (n=25), and sLOX ‐1 level positively correlated with L5 level in AMI patients. Conclusions The level of LOX ‐1 and the ratio of sLOX ‐1 to membrane‐bound LOX ‐1 in aspirated thrombi, as well as the circulating level of sLOX ‐1 were higher in STEMI patients than in non–ST‐segment–elevation myocardial infarction patients. L5 may play a role in releasing a high level of sLOX ‐1 into the circulation of STEMI patients.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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