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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
Published on: August 2, 2018
Hypoxia Modulates Sodium Chloride Co-transporter via CaMKII-β Pathway: An In Vitro Study with mDCT15 Cells
Lijuan Liang1, Kohei Ueda2, Sayoko Ogura3
1Department of Clinical Laboratory, International University of Health and Welfare, Chiba 286-8686, Japan.
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 (CoCl2) 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 CoCl2-induced hypoxia. KN93 reversed the effect of CoCl2 on NCC and phosphorylated NCC expression.
Conclusions:
Hypoxia, mediated through cobalt chloride treatment, upregulates NCC expression via the CaMKII-β pathway in mDCT15 cells.
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