Kim Minjoo, Lee Hyun-Kyung, Lee Hongchan, Lee Hyun-Shik
KNU G-LAMP Project Group, KNU Institute of Basic Sciences, School of Biotechnology, BK21 FOUR KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Daegu, Republic of Korea.
Anim Cells Syst (Seoul). 2025 Jul 16;29(1):438-445. doi: 10.1080/19768354.2025.2533823. eCollection 2025.
Peroxiredoxin6 (Prdx6) is a bifunctional antioxidant enzyme with both peroxidase and phospholipase A₂ activities. Although its molecular roles are well established, the developmental role of Prdx6 remains poorly understood. To address this gap in the literature, this study aimed to examine the function of Prdx6 in primitive myelopoiesis using embryos. We found that is specifically expressed in myeloid progenitors originating from the anterior ventral blood island during early embryogenesis. Knockdown of significantly reduced the number of myeloid cells, without affecting their migration ability. Embryos depleted of exhibited elevated levels of reactive oxygen species (ROS) and decreased cellular proliferation. Co-injection of morpholino (MO)-resistant mRNA or treatment with N-acetylcysteine (NAC) successfully restored both ROS levels and myeloid cell numbers, suggesting that Prdx6 supports primitive myeloid cell development by maintaining redox homeostasis. These findings reveal a novel role of Prdx6 in ROS-dependent proliferation of myeloid progenitors during early vertebrate development.
过氧化物酶体增殖物激活受体6(Prdx6)是一种具有过氧化物酶和磷脂酶A₂活性的双功能抗氧化酶。尽管其分子作用已得到充分证实,但Prdx6在发育过程中的作用仍知之甚少。为了填补文献中的这一空白,本研究旨在利用胚胎研究Prdx6在原始髓系造血中的功能。我们发现,在胚胎早期发育过程中,Prdx6在源自前腹侧血岛的髓系祖细胞中特异性表达。敲低Prdx6显著减少了髓系细胞的数量,但不影响其迁移能力。缺乏Prdx6的胚胎表现出活性氧(ROS)水平升高和细胞增殖减少。共注射抗吗啉代寡核苷酸(MO)的Prdx6 mRNA或用N-乙酰半胱氨酸(NAC)处理成功恢复了ROS水平和髓系细胞数量,这表明Prdx6通过维持氧化还原稳态来支持原始髓系细胞的发育。这些发现揭示了Prdx6在早期脊椎动物发育过程中对髓系祖细胞ROS依赖性增殖的新作用。