CD40 Ligand and Its Receptors in Atherothrombosis

Yacoub, Daniel; Hassan, Ghada S.; Alaadine, Nada; Merhi, Yahye; Mourad, Walid

doi:10.5772/33289

Cited by 1 publication

(1 citation statement)

References 102 publications

(116 reference statements)

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“…Taken together with various other reports showing that proteasome inhibition reduces platelet aggregation and/or secretion only in presence of low doses of platelet agonists [ 69 , 104 , 108 , 126 , 131 , 149 ], it can be speculated that the proteasome/NF-κB dyad does not regulate platelet activation but rather platelet priming, in which platelets are not fully activated to aggregate (no Ca2+ influx or strong αIIbβ3 activation) but present with activation markers including P-selectin exposure and dynamic cytoskeletal shape changes [ 155 , 156 , 157 ]. Eventually, platelet priming potentiates platelet activation and aggregation when low doses of platelet agonists are secured [ 53 , 133 , 134 , 156 , 158 , 159 ].…”

Section: Nf-κb/proteasome Coupling In Plateletsmentioning

confidence: 99%

The Role of the Proteasome in Platelet Function

El-Kadiry

Merhi

2021

IJMS

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Platelets are megakaryocyte-derived acellular fragments prepped to maintain primary hemostasis and thrombosis by preserving vascular integrity. Although they lack nuclei, platelets harbor functional genomic mediators that bolster platelet activity in a signal-specific manner by performing limited de novo protein synthesis. Furthermore, despite their limited protein synthesis, platelets are equipped with multiple protein degradation mechanisms, such as the proteasome. In nucleated cells, the functions of the proteasome are well established and primarily include proteostasis among a myriad of other signaling processes. However, the role of proteasome-mediated protein degradation in platelets remains elusive. In this review article, we recapitulate the developing literature on the functions of the proteasome in platelets, discussing its emerging regulatory role in platelet viability and function and highlighting how its functional coupling with the transcription factor NF-κB constitutes a novel potential therapeutic target in atherothrombotic diseases.

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