Fujiwara Tohru
Department of Laboratory Medicine & Infectious Diseases, Iwate Medical University School of Medicine.
Rinsho Ketsueki. 2024;65(3):183-187. doi: 10.11406/rinketsu.65.183.
The transcription factor GATA-1 is essential for erythroid differentiation. Recently, FAM210B, which encodes a mitochondrial inner membrane protein, has been identified as a novel target of GATA-1. To clarify the role of FAM210B, we depleted endogenous FAM210B in human iPS-derived erythroid progenitor (HiDEP-1) cells, and found that erythroid differentiation was more pronounced in the FAM210B depleted cells. Comprehensive metabolite analysis revealed a decline in mitochondrial function accompanied by increased lactate production, indicative of anaerobic glycolysis. Mass spectrometry revealed that FAM210B could interact with multiple subunits of mitochondrial ATP synthases, such as subunit alpha (ATP5A) and beta (ATP5B). Our results suggested that FAM210B contributes prominently to erythroid differentiation by regulating mitochondrial energy metabolism. This review will discuss the potential association between mitochondrial metabolism and erythropoiesis.
转录因子GATA-1对红细胞分化至关重要。最近，编码线粒体内膜蛋白的FAM210B已被确定为GATA-1的一个新靶点。为了阐明FAM210B的作用，我们在人诱导多能干细胞衍生的红细胞祖细胞（HiDEP-1）中耗尽了内源性FAM210B，发现FAM210B耗尽的细胞中红细胞分化更为明显。综合代谢分析显示线粒体功能下降，同时乳酸生成增加，这表明存在无氧糖酵解。质谱分析表明，FAM210B可与线粒体ATP合酶的多个亚基相互作用，如α亚基（ATP5A）和β亚基（ATP5B）。我们的结果表明，FAM210B通过调节线粒体能量代谢对红细胞分化有显著贡献。本综述将讨论线粒体代谢与红细胞生成之间的潜在关联。
