TRP channel function in platelets and megakaryocytes: basic mechanisms and pathophysiological impact

Abstract

Transient receptor potential (TRP) proteins form a superfamily of cation channels that are expressed in a wide range of tissues and cell types. During the last years, great progress has been made in understanding the molecular complexity and the functions of TRP channels in diverse cellular processes, including cell proliferation, migration, adhesion and activation. The diversity of functions depends on multiple regulatory mechanisms by which TRP channels regulate Ca²⁺ entry mechanisms and intracellular Ca²⁺ dynamics, either through membrane depolarization involving cation influx or store- and receptor-operated mechanisms. Abnormal function or expression of TRP channels results in vascular pathologies, including hypertension, ischemic stroke and inflammatory disorders through effects on vascular cells, including the components of blood vessels and platelets. Moreover, some TRP family members also regulate megakaryopoiesis and platelet production, indicating a complex role of TRP channels in pathophysiological conditions. In this review, we describe potential roles of TRP channels in megakaryocytes and platelets, as well as their contribution to diseases such as thrombocytopenia, thrombosis and stroke. We also critically discuss the potential of TRP channels as possible targets for disease prevention and treatment.

Keywords: Megakaryocytes; Platelets; Receptor-operated Ca(2+) entry (ROCE); Store-operated Ca(2+) entry (SOCE); Stroke; TRP channels; Thrombosis.