细胞表面GRP78:高葡萄糖诱导的内皮损伤的潜在治疗点
Bo Wang1, Xin He1, Jingliang Zhang1
1First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, China.
Biochemical and biophysical research communications
|December 6, 2023
概括
向细胞表面GRP78 (葡萄糖调节蛋白78) 可以减少内皮细胞的炎症和氧化应激,为糖尿病血管并发症提供潜在的治疗方法.
科学领域:
- 生物医学研究的研究.
- 细胞生物学 细胞生物学
- 血管医学是一种血管医学.
背景情况:
- 内皮细胞炎症和氧化应激是糖尿病血管并发症的关键因素.
- 细胞表面GRP78在这些过程中的作用尚未完全理解.
研究的目的:
- 调查抑制细胞表面GRP78是否可以抑制高葡萄糖诱导的内皮炎症和氧化应激.
- 探索细胞表面GRP78影响这些条件的机制.
主要方法:
- 利用一种新的抗GRP78单克隆抗体 (MAb159) 来抑制细胞表面GRP78的功能.
- 用高葡萄糖 (HG) 治疗人类静脉内皮细胞 (HUVECs).
- 评估了MAb159和重组GRP78对内皮损伤,炎症和氧化应激标志物的影响.
主要成果:
- 高葡萄糖增加了HUVECs中的细胞表面GRP78表达.
- MAb159治疗减轻了HG诱导的内皮损伤,炎症和氧化应激.
- 再组合GRP78加剧了HG诱导的内皮损伤.
- 细胞表面GRP78激活TLR4/NF-κB信号通路,促进炎症和氧化应激.
- 由HG诱导的GRP78转位取决于ER压力.
结论:
- 细胞表面GRP78在促进高葡萄糖诱导的内皮炎症和氧化应激方面发挥着重要作用.
- 抑制细胞表面GRP78功能是糖尿病血管并发症的潜在治疗策略.
- 针对GRP78转位,可能通过ER应力调制,可以减轻内皮损伤.
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