Beta-Glycerophosphate-Induced ORAI1 Expression and Store Operated Ca²⁺ Entry in Megakaryocytes.

ABSTRACT: Impairment of renal phosphate elimination in chronic kidney disease (CKD) leads to enhanced plasma and tissue phosphate concentration, which in turn up-regulates transcription factor NFAT5 and serum & glucocorticoid-inducible kinase SGK1. The kinase upregulates ORAI1, a Ca²⁺-channel accomplishing store-operated Ca²⁺-entry (SOCE). ORAI1 is stimulated following intracellular store depletion by Ca²⁺-sensors STIM1 and/or STIM2. In megakaryocytes and blood platelets SOCE and thus ORAI1 are powerful regulators of activity. The present study explored whether the phosphate-donor ß-glycerophosphate augments NFAT5, ORAI1,2,3 and/or STIM1,2 expressions and thus SOCE in megakaryocytes. Human megakaryocytic Meg01cells were exposed to 2 mM of phosphate-donor ß-glyceropho

SUBMITTER: Pelzl L 

PROVIDER: S-EPMC6997179 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature