<b>Heat-shock protein 72 promotes platelet aggregation induced by various platelet activators in </b><b>rats </b>

Abstract

Increase of thrombus in the coronary arteries is positively correlated with the level of heat-shock protein 72 (HSP72) in the blood of patients with acute myocardial infarction (AMI). Platelet aggregation participates in thrombus formation on ruptured plaque in AMI. In this study, we aimed to clarify the role of HSP72 in thrombus formation by evaluating the effects of HSP72 on platelet aggregation. Platelet aggregation activities were measured in platelet-rich plasma obtained from male Sprague-Dawley rats with or without the platelet activators, such as adenosine diphosphate (ADP), collagen, thrombin receptor-activating peptide-6 (TRAP-6), ristocetin, and arachidonic acid. Changes in aggregation were estimated by the co-addition of recombinant HSP72 and anti-HSP72 antibodies. Our results showed that addition of HSP72 increased platelet aggregation in the presence of low concentrations of ADP, collagen, TRAP-6, ristocetin, and arachidonic acid. Increased platelet aggregation stimulated by ADP and HSP72 was reduced by the co-addition of anti-HSP72 antibodies. Thus, these findings suggested that HSP72 was released extracellularly in response to stress, promoting thrombus formation and AMI. Additionally, treatment with anti-HSP72 antibodies may control platelet aggregation induced by extracellular HSP72.

The Value of SIRT1/FOXO1 Signaling Pathway in Early Detection of Cardiovascular Risk in Children with β-Thalassemia Major

“…Bobryshev et al [ 58 ] found that HSP70 was expressed even in dendritic cells in the arterial wall and indicated that elevated HSPs in plaque cells, particularly macrophages, were more stressed within the depth of the atheroma, especially in association with necrosis. In contrast, Suzuki et al [ 59 ] stated that patches of smooth muscle cells were observed in the most complex plaques but without consistent association with necrosis or increased HSP70. Such aforementioned relationships emphasize furthermore the importance of assessed HSP 72 increments in association with their inflammatory-induced response to ROS via the impact of plasma ferritin increments that promote atherogenicity in β-TM under study.…”

Genetic Deletion of HLJ1 Does Not Affect Blood Coagulation in Mice

“…HSP70 regulates platelet integrin activation, granule secretion and aggregation [29]. Suzuki et al demonstrated that HSP72 promotes activatorinduced platelet aggregation [24]. Very recently, Jackson et al (2020) reported that the inhibition of HSP40 and HSP90 by pharmacological antagonists abolishes the dense granule release, thromboxane synthesis and aggregation in thrombin-treated platelets [30].…”

“…Recent studies have identified the role of HSPs in the blood coagulation of mammals [22,23]. For example, HSP72 promotes platelet aggregation, and HSP20 plays a vital role in coagulation function [24,25]. While the role of HLJ1 in cancer biology has been extensively investigated, its significance in blood coagulation is still elusive.…”