新型亚细胞结构血红蛋白小体增强软骨细胞的缺氧耐受  

Hemoglobin Body as a Novel Subcellular Structure Enhances Chondrocyte Hypoxia Adaption

作　　者：张波 孙强 ZHANG Bo;SUN Qiang(Laboratory of Cell Engineering,Institute of Biotechnology,Academy of Military Medical Science,Beijing 100071,China;Research Unit of Cell Death Mechanism(2021RU008),Chinese Academy of Medical Science,Beijing 100071,China;Nanhu Laboratory,Jiaxing 314002,China)

机构地区：[1]细胞工程研究室,生物工程研究所,军事医学研究院,北京100071 [2]细胞死亡机制创新单元(2021RU008),中国医学科学院,北京100071 [3]南湖实验室,嘉兴314002

出　　处：《中国细胞生物学学报》2024年第6期1063-1069,共7页Chinese Journal of Cell Biology

基　　金：中国博士后科学基金(批准号:2023M744312);国家重点研发计划(批准号:2022YFC3600100);中国医学科学院创新工程(批准号:2021-I2M-5-008)资助的课题。

摘　　要：最近的研究显示,作为氧气载体的血红蛋白在软骨细胞中大量产生,并且可以通过液–液相分离(liquid-liquid phase separation,LLPS)的方式聚合成血红蛋白小体(hemoglobin body,hedy)这一全新的细胞结构。软骨细胞中血红蛋白的产生依赖于Klf1而不是传统的Hif1/2α途径。敲除软骨细胞中的血红蛋白会导致软骨生长板缺氧加剧以及软骨组织中心区域广泛的细胞死亡。这一工作揭示了软骨细胞耐受缺氧的新机制,即hedy可作为氧气储备和应急供应结构促进软骨细胞的存活。Recent study indicates that massive amounts of hemoglobin,a known carrier of oxygen in erythrocytes,is produced in chondrocyte,where it can form a new structure hedy(hemoglobin body)by liquid-liquid phase separation.The production of hemoglobin in chondrocytes turns out to be dependent on Klf1 rather than the classical Hif1/2αpathway.Hemoglobin depletion leads to enhanced hypoxia that causes extensive cell death in the center of cartilaginous tissue.These results demonstrate uncover a heretofore unrecognized mechanism whereby chondrocytes survive a hypoxic environment on hedy,an oxygen storage for emergency supply.

关 键 词：血红蛋白小体 软骨细胞 血红蛋白 Klf1 相分离 

分 类 号：R681.3[医药卫生—骨科学]