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Oxygen Glucose Deprivation-induced Apoptosis in Oligodendrocytes Through TRPC3 |
MENG Zan, XU Dan, LI Zhen, LI Jing, LI Gang, LIU Yong-gang, LIU Zhao yu, WU Hong, TANG Yong, PENG Yan |
Department of Histology and Embryology, Laboratory of Stem Cell and Tissue Engineering, College of Basic Medicine, Chongqing Medical University, Chongqing 400016, China |
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Abstract Objective: To explore whether transient receptor potential canonical 3 (TRPC3) plays a role in the apoptosis of oligodendrocytes induced by oxygen glucose deprivation(OGD).Methods: Control group were established by primary cultured oligodendrocytes of SD rats,model group were established by primary cultured oligodendrocytes of SD rats which exposed to OGD2h,treated group were established by model group+ Pyr3.Western blotting were used to detect the expression of TRPC3 at protein levels.The viability of the oligodendrocytes was determined by MTT assay,and the apoptosis of oligodendrocytes were measured by flow cytometry after AnnexinV-FITC staining,intracellular Ca2+ concentration were measured by flow cytometry and Laser Confocal Scamfing Microscope(LCSM).Results: Specific markers of A2B5 and MBP in oligodendrocytes were positive and the purification is more than 95%,OGD model was established successfully.A significant increase in the expression of TRPC3 in cultured oligodendrocytes.The viability of OGD oligodendrocytes (54.34±6.55)% was obviously decreased and the apoptosis rate was increased (24.24±0.86)% when compared with the control cells (P<0.05).Pyr3 significantly increased the survival rate (72.26±5.41)% and decreased the apoptosis rate (14.82±0.28)% and partially suppressed Ca2+ in oligodendrocytes (P<0.05).Conclusion: The increased expression of TRPC3 which mediated intracellular calcium level may be one of the important reasons for OGD oligodendrocyte apoptosis.
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Received: 05 February 2015
Published: 25 April 2015
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Cite this article:
MENG Zan, XU Dan, LI Zhen, LI Jing, LI Gang, LIU Yong-gang, LIU Zhao yu, WU Hong, TANG Yong, PENG Yan. Oxygen Glucose Deprivation-induced Apoptosis in Oligodendrocytes Through TRPC3. China Biotechnology, 2015, 35(4): 23-29.
URL:
https://manu60.magtech.com.cn/biotech/10.13523/j.cb.20150404 OR https://manu60.magtech.com.cn/biotech/Y2015/V35/I4/23
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[1] Tang Y,Nyengaard J R,Pakkenberg B,et al.Age-induced white matter changes in the human brain:a stereological investigation.Neurobiol Aging,1997,18(6):609-615.
[2] 张蕾,卢伟,闵琦珵,等.大鼠大脑海马结构内有髓神经纤维髓鞘老年性改变的体视学研究.第三军医大学学报,2010,32(19):2053-2057. Zhang L, Lu W, Min Q, et al. Age-related changes in myelin sheaths of myelinated fibers in rat hippocampus:a stereological study. Acta Academiae Medicinae Militaris Tertiae, 2010,32(19):2053-2057.
[3] Mifsud G,Zammit C,Muscat R,et al.Oligodendrocyte pathophysiology and treatment strategies in cerebral ischemia.CNS Neurosci Ther,2014,20(7):603-612.
[4] McTigue D M,Tripathi R B.The life,death,and replacement of oligodendrocytes in the adult CNS.J Neurochem,2008,107(1):1-19.
[5] McCormack J G.Role of calcium ions in regulation of mammalian intramitochondrial metabolism.Physiol Rev,1990,70(2):391-425.
[6] Orrenius S,Zhivotovsky B,Nicotera P.Regulation of cell death:the calcium-apoptosis link.Nat Rev Mol Cell Biol,2003,4(7):552-565.
[7] Bezprozvanny I.Calcium signaling and neurodegenerative diseases.Trends Mol Med,2009,15(3):89-100.
[8] Marambaud P,Dreses W U,Vingtdeux V.Calcium signaling in neurodegeneration.Mol Neurodegener,2009,4:20.
[9] RA R,DD B,MM M,et al.Ca2+ entry through TRPC channels regulates fibroblast biology in chronic atrial fibrillation.Circulation,2012,126(17):2039-2041.
[10] Cvetkovic-Lopes V,Eggermann E,Uschakov A,et al.Rat hypocretin/orexin neurons are maintained in a depolarized state by TRPC channels.PLoS One,2010,5(12):e15673.
[11] 丁月,肖楚瑶,蒋建敏.瞬时感受器电位通道与疾病 [J] .现代生物医学进展,2008,8(12): 2381-2384. Ding Y,Xiao C Y,Jiang J M. Transient receptor potential channel and disease. Progress in Modern Biomedicine,2008,8(12): 2381-2384.
[12] Chen Y,Balasubramaniyan V,Peng J,et al.Isolation and culture of rat and mouse oligodendrocyte precursor cells.Nat Protoc,2007,2(5):1044-1051.
[13] Niu J,Wang L,Liu S,et al.An efficient and economical culture approach for the enrichment of purified oligodendrocyte progenitor cells.J Neurosci Methods,2012, 209(1):241-249.
[14] Zhu B,Zhao C,Young F I,et al.Isolation and long-term expansion of functional, myelinating oligodendrocyte progenitor cells from neonatal rat brain.Curr Protoc Stem Cell Biol,2014,31:2D.17.1~2D.17.15.
[15] Cicchetti F,Barker R A. The glial response to intracerebrally delivered therapies for neurodegenerative disorders: is this a critical issue? Front Pharmacol,2014, 5:139.
[16] Cui Q L,Kuhlmann T,Miron V E,et al.Oligodendrocyte progenitor cell susceptibility to injury in multiple sclerosis.Am J Pathol,2013, 183(2):516-525.
[17] Du Y,Dreyfus C F.Oligodendrocytes as providers of growth factors.J Neurosci Res,2002,68(6):647-654.
[18] Kuzdas D,Stemberger S,Gaburro S, et al. Oligodendroglial alpha-synucleinopathy and MSA-like cardiovascular autonomic failure:experimental evidence. Exp Neurol, 2013,247:531-536.
[19] 姜茜,姜玉武,王静敏,等.一种改进的大鼠皮层神经元原代培养方法及其性质鉴定. 北京大学学报(医学版),2009,02:212-216. Jiang X,Jiang Y W,Wang J M,et al.An improved method for primary culture of rat cortical neuron and cell identification.Journal of Peking University(Health Sciences),2009,02:212-216.
[20] 文莉莉,米永杰,陈纯海,等.TRPC3参与电磁辐射致培养的海马神经元凋亡.第三军医大学学报,2013,35(6):491-494. Wen L L,Mi Y J,Chen C H,et al.Electromagnetic irradiation- induced apoptosis in hippocampal neurons through.Journal of Third Military Medical University,2013,35(6):491-494.
[21] 王岩,王莎莉,赵香琴,等.TRPC通道对PC12细胞缺氧缺糖再灌注后氧化损伤的保护作用.中国生物化学与分子生物学报,2014,01:85-92. Wang Y,Wang S L,Zhao X Q,et al. Protective of transient receptor potential canonical on oxygen-glucose deprivation/reperfusion (OGD-R)-induced injury in PC12 cells.Chinese Journal of Biochemistry and Molecular Biology, 2014,01:85-92.
[22] Selvaraj S,Sun Y.TRPC channels and their implication in neurological diseases.CNS Neurol Disord Drug Targets,2010,9(1):94-104.
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