Proplatelet formation in megakaryocytes is associated with endoplasmic reticulum stress.
Although previous studies suggest that proplatelet formation in megakaryocytes involves caspase-3, the mechanism underlying the activation of caspase-3 is unknown. Here, we analyzed caspase activation in a human megakaryoblastic cell line, MEG-01, which forms proplatelets spontaneously. Specific activation of caspase-3 and caspase-4 was found in proplatelets. Consistent with previous observations of caspase-4 autoactivation in response to endoplasmic reticulum (ER) stress, several ER stress marker proteins were expressed during proplatelet formation. A pharmacological ER stressor enhanced platelet production via proplatelet formation, whereas inhibition of caspase-4 caused suppression. These results suggest that ER stress is a mechanism underlying the maturation of megakaryocytes.
Lipid Biology Laboratory, RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan.
Nobuhiro
N
Morishima
Lipid Biology Laboratory, RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan.
Keiko
K
Nakanishi
D017209:Apoptosis / Q000235:genetics; D001792:Blood Platelets / Q000378:metabolism; D053148:Caspase 3 / Q000096:biosynthesis* / Q000235:genetics; D053471:Caspases, Initiator / Q000096:biosynthesis* / Q000235:genetics; D002478:Cells, Cultured; D059865:Endoplasmic Reticulum Stress / Q000235:genetics*; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D008533:Megakaryocytes / Q000378:metabolism*
C093516:CASP4 protein, human; D053148:Caspase 3; D053471:Caspases, Initiator