USP5 通过通过二氧化化稳定ROBO4,促进糖尿病视网膜病变的发展
Hao Guo1, Ruibao Liu2, Haijiang Lv2
1Eye School of Chengdu University of TCM, Chengdu, China; Department of Ophthalmology, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Cellular signalling
|May 12, 2024
概括
乌比基特异蛋白酶5 (USP5) 通过稳定ROBO4.4而加剧糖尿病视网膜病变. 在高葡萄糖条件下,USP5促进细胞损伤,炎症和细胞亡,有助于疾病的进展.
科学领域:
- 眼科医生 眼科 眼科
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 糖尿病视网膜病变 (DR) 是糖尿病的一个微血管并发症.
- 乌比基特异性蛋白酶 (USP) 参与了DR的病变发生.
- 在DR中USP5的具体作用尚不清楚.
研究的目的:
- 研究USP5在糖尿病视网膜病变中的作用.
- 阐明USP5在高葡萄糖诱导的视网膜细胞损伤中的潜在机制.
主要方法:
- 人类视网膜色素上皮质 (HRPE) 细胞被用来建模DR.
- 评估了细胞增殖,细胞亡,炎症和氧化应激.
- 通过RT-qPCR和西部斑块测量了USP5和ROBO4的表达.
- 进行了共免疫沉和二氧化定位测试.
主要成果:
- 高葡萄糖 (HG) 诱导HRPE细胞损伤,包括抑制增殖和增加亡,炎症和氧化应激.
- 在DR患者的血和HG治疗的HRPE细胞中,USP5和ROBO4都被上调.
- USP5通过duebiquitination稳定了ROBO4,加剧了HG诱导的HRPE细胞损伤.
- 通过降低ROBO4水平,USP5敲击减轻了HG诱导的细胞损伤.
结论:
- USP5在促进糖尿病视网膜病变的发展方面发挥着至关重要的作用.
- USP5通过二化稳定ROBO4,导致HRPE细胞功能障碍.
- 针对USP5可能为糖尿病视网膜病变提供治疗策略.
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