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糖尿病病中近端管状细胞中的高CD133表达:好还是坏?

Yuhan Zhang^1,2,3, Lusi Xu¹, Congcong Guo¹

¹Department of Endocrinology and Metabology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, 250014, China.

Journal of translational medicine

|February 16, 2024

概括

在糖尿病病 (DKD) 中,CD133上调最初有助于近接管状细胞存活,但持续增加与DKD进展相关,表明其具有双重作用.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

糖尿病病 (DKD) 涉及近端管状细胞 (PTC).
CD133是一种原始标记物,涉及急性损伤再生,但其在慢性损伤中的作用尚不清楚.
研究CD133在DKD中的表达和功能至关重要.

研究的目的:

在糖尿病病 (DKD) 中研究CD133在近接管状细胞 (PTC) 的表达模式.
阐明CD133在DKD进展中的功能意义.
了解CD133在高葡萄糖诱导的PTC损伤和DKD病变中的双重作用.

主要方法:

使用数据挖掘,大鼠DKD模型,以及人类 (HK-2) 和大鼠 (NRK-52E) PTC.
通过免疫光和流细胞计评估了CD133的表达.
通过基因过度表达/敲击,EDU测定,实时细胞分析和西斑/RT-PCR来研究CD133的功能.

主要成果:

在DKD PTC中,CD133表达升高,随着疾病的进展而增加.
CD133与KIM-1和PCNA等标记物的共同表达表明了细胞损伤和增殖.
CD133倒置增加了亡;过度表达减少了亡,但在高葡萄糖条件下没有扩散.
单细胞RNA测序数据表明CD133+ PTC通过多种途径对DKD作出贡献.

结论:

升级的CD133促进PTC增殖,并保护DKD和高葡萄糖损伤中的细胞亡.
增加的CD133可能提供初始的自我保护,但持续增加与DKD进展有关.
CD133在DKD中表现出双重作用,需要进一步研究.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.CD133 是一个CD133 CD133 是一个CD133 数据挖掘是一种数据挖掘.糖尿病脏疾病糖尿病脏疾病靠近的管状细胞.

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