What can we learn from senescent platelets, their transcriptomes and proteomes?

Abstract

Research into the natural aging process of platelets has garnered much research interest in recent years, and there have long been associations drawn between the proportion of newly formed platelets in the circulation and the risk of thrombosis. However, these observations have largely been demonstrated in patient groups in which there may be underlying systemic changes that effect platelet function. Recent advances in technology have allowed in-depth analysis of differently aged platelets isolated from the peripheral blood of healthy individuals and have demonstrated that aged platelets, often referred to as senescent platelets, undergo extensive changes in the transcriptome and proteome. Ultimately, these changes result in platelets whose functions have deteriorated such that they cannot partake in hemostatic responses to the same extent as newly formed platelets. Here, we review transcriptomic and proteomic research in platelet aging in the context of health and how this research sheds light upon alterations in platelet structure and function.

The Effect of Leukocyte Removal and Matrix Metalloproteinase Inhibition on Platelet Storage Lesions

“…During the storage of the PCs, adverse changes in platelets—PSLs—occur [ 38 ]. The reasons why platelets lose their ability to aggregate and undergo intensified activation during storage remain unclarified [ 5 , 14 ]. Platelets, plasma and leukocytes present in the PC contain and release, inter alia, extracellular matrix metalloproteinases that affect the activity of platelets [ 25 ].…”

“…It has been reported that factors leading to platelet activation and damage include contact with a charged surface, changes in temperature and oxygen availability, and the presence of leukocytes and erythrocytes, cellular debris and enzymes. Researchers have studied the contents of RANTES, TGF-β, INF-γ, IL-1, IL-6, and IL-8 in PCs; the extracellular accumulation of histamine, PAI-1,VEGF and IL-6; and platelet lipid profile changes [ 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 ]. Changes in pH and changes in the concentration of lactate dehydrogenase, which is used as a marker of cell damage in cell cultures, were analyzed as potential causes of increased platelet activation [ 15 , 16 , 17 , 18 , 19 , 20 ].…”