Highly oxidized low-density lipoprotein does not facilitate platelet aggregation

• Published in: Journal of international medical research 2020-10, Vol.48 (10), p.300060520958960-300060520958960
• Main Authors: Miyazaki, Akari, Uehara, Takeshi, Usami, Yoko, Ishimine, Nau, Sugano, Mitsutoshi, Tozuka, Minoru
• Format: Article
• Language: English
• Subjects: Adenosine Diphosphate - pharmacology; Atherosclerosis; Blood Platelets; Cardiovascular disease; Lipoproteins, LDL; Low density lipoprotein; Oxidation; Platelet Aggregation; Pre-Clinical Research Report
• ISSN: 0300-0605; 1473-2300
• DOI: 10.1177/0300060520958960

Objective This study aimed to examine whether oxidized low-density lipoprotein (oxLDL) facilitates platelet aggregation, which is one cause for development of cardiovascular disease. Methods The susceptibility of platelets to aggregation was monitored by light transmittance aggregometry and a laser light scattering method using low-density lipoprotein (LDL) and oxLDL as agonists. β-thromboglobulin (β-TG) levels released from platelets were also measured after incubation with or without oxLDL. Results Platelet aggregation was suppressed by oxLDL as estimated by maximum light transmission. Additionally, adenosine diphosphate-induced further aggregation was slightly reduced by the presence of oxLDL. Aggregation levels of a low number of platelets, which was determined by the laser light scattering method, were lower upon addition of oxLDL compared with unoxidized LDL. After a short time of incubation, oxLDL increased secreted β-TG levels in platelet-rich plasma. However, further incubation with oxLDL caused relatively lower secreted β-TG levels compared with incubation with unoxidized LDL. This fluctuation was not due to β-TG degradation by oxLDL. Conclusions Levels of oxLDL in vitro weakly activate platelets at an early stage, but then inhibit platelet function, such as aggregation and β-TG secretion.