Li Zeyu, Han Delong, Li Zhenchi, Luo Lingjie
College of Pharmaceutical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.
Marshall Laboratory of Biomedical Engineering, Institute for Inheritance-Based Innovation of Chinese Medicine, Shenzhen University Medical School, Shenzhen 518055, China.
Biology (Basel). 2024 Aug 8;13(8):598. doi: 10.3390/biology13080598.
Animal embryonic development occurs under hypoxia, which can promote various developmental processes. Embryonic fibroblasts, which can differentiate into bone and cartilage and secrete various members of the collagen protein family, play essential roles in the formation of embryonic connective tissues and basement membranes. However, the adaptations of embryonic fibroblasts under hypoxia remain poorly understood. In this study, we investigated the effects of hypoxia on mouse embryonic fibroblasts (MEFs). We found that hypoxia can induce migration, promote metabolic reprogramming, induce the production of ROS and apoptosis, and trigger the activation of multiple signaling pathways of MEFs. Additionally, we identified several hypoxia-inducible genes, including , , , , and , which are regulated by HIF1α. Furthermore, we demonstrated that CoCl partially mimics the effects of low oxygen on MEFs. However, we found that the mechanisms underlying the production of ROS and apoptosis differ between hypoxia and CoCl treatment. These findings provide insights into the complex interplay between hypoxia, fibroblasts, and embryonic developmental processes.
动物胚胎发育在缺氧条件下发生,缺氧可促进各种发育过程。胚胎成纤维细胞可分化为骨和软骨并分泌胶原蛋白家族的各种成员,在胚胎结缔组织和基底膜的形成中起重要作用。然而,缺氧条件下胚胎成纤维细胞的适应性仍知之甚少。在本研究中,我们研究了缺氧对小鼠胚胎成纤维细胞(MEFs)的影响。我们发现缺氧可诱导迁移、促进代谢重编程、诱导活性氧(ROS)产生和细胞凋亡,并触发MEFs多种信号通路的激活。此外,我们鉴定了几个缺氧诱导基因,包括 、 、 、 和 ,它们受缺氧诱导因子1α(HIF1α)调控。此外,我们证明氯化钴(CoCl)部分模拟了低氧对MEFs的影响。然而,我们发现缺氧和CoCl处理之间ROS产生和细胞凋亡的潜在机制有所不同。这些发现为缺氧、成纤维细胞和胚胎发育过程之间的复杂相互作用提供了见解。