Proplatelet formation from megakaryocytes is associated with endoplasmic reticulum stress
Proplatelet formation from megakaryocytes is associated with endoplasmic reticulum stress
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巨核细胞的前血小板形成与内质网应激有关
DOI：
10.1111/gtc.12384
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发表时间：
2016
期刊：
影响因子：
2.1
通讯作者：
Nobuhiro Morishima and Keiko Nakanishi
中科院分区：
文献类型：
--
作者：
松岡里実;上田昌宏;Nobuhiro Morishima and Keiko Nakanishi
虽然先前的研究表明巨核细胞中的前血小板形成涉及caspase-3，但caspase-3激活的潜在机制尚不清楚。在这里，我们分析了人巨核细胞系MEG-01中的半胱天冬酶激活，该细胞系自发形成前血小板。在前血小板中发现了caspase-3和caspase-4的特异性活化。与先前观察到的响应内质网（ER）应激的caspase-4自激活一致，在前血小板形成期间表达了几种ER应激标志物蛋白。药理学ER应激因子通过前血小板形成增强血小板生成，而caspase-4的抑制引起抑制。这些结果表明，ER应激是巨核细胞成熟的一种机制。
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.