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Bumetanide-induced NKCC1 inhibition attenuates oxygen-glucose deprivation-induced decrease in proliferative activity and cell cycle progression arrest in cultured OPCs via p-38 MAPKs

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单位: [1]Huazhong Univ Sci & Technol,Tongji Med Coll,Tongji Hosp,Dept Neurol,Wuhan 430030,Peoples R China [2]Minist Educ China, Key Lab Neurol Dis HUST, Wuhan 430030, Peoples R China
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关键词: OPCs Na-K-Cl co-transporter 1 (NKCC1) Oxygen/glucose deprivation (OGD) Cell cycle

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The Na-K-Cl co-transporter 1 (NKCC1; a member of the cation-chloride co-transporter family) mediates the coupled movement of Na+ and/or K+ with Cl- across the plasma membrane of cells (Haas and Forbush, 2000, Annu. Rev. Physiol., 62, 515-534; Russell, 2000, Physiol. Rev., 80, 211-276). Although it acts as an important regulator of cell volume, secretion, and modulator of cell apoptosis and proliferation (Chen et al., 2005,J. Cereb. Blood Flow Metab., 25, 54-66; Kahle et al., 2008, Nat. Clin. Pract. Neurol., 4, 490-503; Kidokoro et al., 2014, Am. J. Physiol. Ren. Physiol., 306, F1155-F1160; Wang et al., 2011, Cell. Physiol. Biochem., 28, 703-714), NKCC1's effects on oligodendrocyte precursor cells (OPCs) have not been characterized. The aim of this study was to investigate whether and to what extent inhibition of NKCC1 alters oxygen glucose deprivation (OGD)-induced cell cycle progression. In the present study, we demonstrated that inhibition of NKCC1 with bumetanide attenuates the decrease in OGD-induced DNA synthesis in cultured OPCs. Western blots showed that NKCC1 inhibition led to an increased expression of cyclin D1, CDK 4, and cyclin E in OGD-treated cells. Furthermore, our results showed bumetanide attenuated the decrease in OGD-induced proliferation and arrest of cell cycle progression via the P-38 MAPK signaling cascade. Thus, NKCC1 plays important roles in the proliferation of OPCs under OGD-induced stress.(C) 2015 Elsevier B.V. All rights reserved.

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出版当年[2014]版:
大类 | 3 区 医学
小类 | 4 区 神经科学
最新[2025]版:
大类 | 4 区 医学
小类 | 4 区 神经科学
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Q3 NEUROSCIENCES
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Q3 NEUROSCIENCES

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第一作者单位: [1]Huazhong Univ Sci & Technol,Tongji Med Coll,Tongji Hosp,Dept Neurol,Wuhan 430030,Peoples R China
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通讯机构: [1]Huazhong Univ Sci & Technol,Tongji Med Coll,Tongji Hosp,Dept Neurol,Wuhan 430030,Peoples R China [2]Minist Educ China, Key Lab Neurol Dis HUST, Wuhan 430030, Peoples R China
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