四川大学Hao Jiang等研究人员合作发现，JunB凝聚可减轻高血糖条件下的血管内皮损伤。该项研究成果于2023年12月22日在线发表在《分子细胞生物学报》上。

研究人员通过ATAC-seq和RNA-seq发现，JunB主要通过细胞周期和p53信号通路逆转了高糖处理的人脐静脉内皮细胞的增殖抑制和凋亡促进作用。此外，JunB在其内在无序区和DNA结合域的介导下，会在细胞核内和体外发生相分离。JunB介导的增殖和凋亡需要核定位和凝聚行为。因此，这项研究揭示了JunB及其凝聚在修复高糖引起的血管内皮损伤中的作用，并阐明了相分离在糖尿病和糖尿病内皮功能障碍中的参与。

据悉，内皮损伤是糖尿病患者血管并发症发生和发展的最初和关键因素，也是导致发病率和死亡率的原因之一。虽然高血糖已被确定为一种损伤效应因子，但其详细机制仍难以捉摸。

附：英文原文

Title: JunB condensation attenuates vascular endothelial damage under hyperglycemic condition

Author: Ren, Xuxia, Cui, Zexu, Zhang, Qiaoqiao, Su, Zhiguang, Xu, Wei, Wu, Jinhui, Jiang, Hao

Issue&Volume: 2023-12-22

Abstract: Endothelial damage is the initial and crucial factor in the occurrence and development of vascular complications in diabetic patients, contributing to morbidity and mortality. Although hyperglycemia has been identified as a damaging effector, the detailed mechanisms remain elusive. In this study, identified by ATAC-seq and RNA-seq, JunB reverses the inhibition of proliferation and the promotion of apoptosis in human umbilical vein endothelial cells treated with high glucose, mainly through the cell cycle and p53 signaling pathways. Furthermore, JunB undergoes phase separation in the nucleus and in vitro, mediated by its intrinsic disordered region and DNA-binding domain. Nuclear localization and condensation behaviors are required for JunB-mediated proliferation and apoptosis. Thus, our study uncovers the roles of JunB and its coacervation in repairing vascular endothelial damage caused by high glucose, elucidating the involvement of phase separation in diabetes and diabetic endothelial dysfunction.

DOI: 10.1093/jmcb/mjad072

Source: https://dx.doi.org/10.1093/jmcb/mjad072