Study on manganese chloride's regulatory mechanism of PHB1 in Z310 cycle arrest and the effect

来源 :2016(第二届)毒性测试替代方法与转化毒理学(国际)学术研讨会暨有害结局路径(AOP)与风险评估培训会议 | 被引量 : 0次 | 上传用户:amy23683
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  The brain parenchyma injury is irreversible in chronic manganism, also early diagnosis and treatment is still difficult.The dopamine neurons are the ultimate target cells of manganese neurotoxicity.The choroid plexus epithelium as one component of blood brain barrier in entricle, synthesize specific nutritional factors for dopamine neurons, namely the growth of the factor 15 (GDF-15), and other ingredients, which secreted to cerebrospinal fluid and sent into the circulatory system.Our previous experiments indicated that Manganese chloride (MnCl2) lead to choroid plexus epithelium cell cycle arrest, and raise the cell cycle regulation related prohibitinl on the level of gene and protein inchoroid plexus epithelium cells.Studies in vitro further confirmed that the upregulation of PHB1 is the main factors in immortalized choroid plexus epithelial cell line Z310 cell cycle block in G1 phase caused by MnCl2.But its molecular mechanism of signal transduction is unknown, and it is unclear that if the choroid plexus epithelium cell cycle arrest caused by MnCl2 could influence the synthesis and secretion of GDF-15, as well as other nutritional factors, consequently detriment the repair of dopamine neurons damage.
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