缺氧通过CaMKII-β途径调节氯化钠协同转运体：mDCT15细胞的体外研究
Hypoxia Modulates Sodium Chloride Co-transporter via CaMKII-β Pathway: An In Vitro Study with mDCT15 Cells.
作者信息
Liang Lijuan, Ueda Kohei, Ogura Sayoko, Shimosawa Tatsuo
机构信息
Department of Clinical Laboratory, International University of Health and Welfare, Chiba 286-8686, Japan.
Department of Physiology, International University of Health and Welfare, Chiba 286-8686, Japan.
出版信息
Life (Basel). 2024 Sep 25;14(10):1229. doi: 10.3390/life14101229.
BACKGROUND
Hypoxia plays a crucial role in regulating various cellular functions, including ion-transport mechanisms in the kidney. The sodium-chloride co-transporter (NCC) is essential for sodium reabsorption in the distal convoluted tubule (DCT). However, the effects of hypoxia on NCC expression and its regulatory pathways remain unclear. We aimed to explore the effects and potential mechanisms of hypoxia on NCC in vitro.
METHODS
mDCT15 cells were treated with cobalt chloride (CoCl) at a concentration of 300 μmol/L to induce hypoxia. The cells were harvested at different time points, namely 30 min, 1 h, 6 h, and 24 h, and the expression of NCC and CaMKII-β was analyzed using Western blot.
RESULTS
A time-dependent upregulation of NCC and CaMKII-β expression in response to CoCl-induced hypoxia. KN93 reversed the effect of CoCl on NCC and phosphorylated NCC expression.
CONCLUSIONS
Hypoxia, mediated through cobalt chloride treatment, upregulates NCC expression via the CaMKII-β pathway in mDCT15 cells.
背景
缺氧在调节多种细胞功能中起关键作用，包括肾脏中的离子转运机制。氯化钠共转运体（NCC）对于远端曲小管（DCT）中的钠重吸收至关重要。然而，缺氧对NCC表达及其调节途径的影响仍不清楚。我们旨在体外探究缺氧对NCC的影响及潜在机制。
方法
用浓度为300μmol/L的氯化钴（CoCl）处理mDCT15细胞以诱导缺氧。在不同时间点（即30分钟、1小时、6小时和24小时）收获细胞，并用蛋白质免疫印迹法分析NCC和CaMKII-β的表达。
结果
对CoCl诱导的缺氧，NCC和CaMKII-β表达呈时间依赖性上调。KN93逆转了CoCl对NCC和磷酸化NCC表达的影响。
结论
通过氯化钴处理介导的缺氧，经由CaMKII-β途径上调mDCT15细胞中的NCC表达。
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