未折叠蛋白反应与神经管缺陷关系的研究进展

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摘要神经管缺陷(neural tube defects,NTDs)是常见的先天性中枢神经系统缺陷,病因复杂。未折叠蛋白反应(unfolded protein response,UPR)是一种早期的针对外界环境因素的应激反应,在神经系统疾病中发挥重要作用,外界环境刺激加剧以及时间延长,UPR会失去作用并启动其他生物效应如细胞自噬、凋亡等。重金属暴露、高热、高糖、必需营养素的缺乏、高同型半胱氨酸血症、PI3K/Akt/GSK-3β通路基因突变等显著增加NTDs发生风险,致病机制不清楚,氧化应激损伤、内质网应激、caspase 8依赖性细胞凋亡及细胞自噬等通路与NTDs发生有关。近年来研究提示线粒体未折叠蛋白反应和内质网未折叠蛋白反应可能在NTDs发生中起重要作用,本文试图从UPR信号通路的角度来探讨外环境暴露导致NTDs发生的作用机制,对于寻找NTDs早期生物标志物及干预靶点具有重要的意义。

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	刘菊芬

关键词 ：未折叠蛋白反应, 氧化应激, 凋亡, 自噬, 神经管缺陷

收稿日期: 2018-11-15

基金资助:国家自然科学基金(81202265)

通讯作者: 刘菊芬(liujufen@bjmu.edu.cn)

引用本文:

刘菊芬. 未折叠蛋白反应与神经管缺陷关系的研究进展[J]. 中国生育健康杂志, 2019, 30(1): 83-87.

链接本文:

http://cjrh.bjmu.edu.cn/CN/ 或 http://cjrh.bjmu.edu.cn/CN/Y2019/V30/I1/83

1 Wallingford JB,Niswander LA,Shaw GM,et al.The continuing challenge of understanding,preventing,and treating neural tube defects.Science,2013,339:1222002.
2 Liu J,Zhang L,Li Z,et al.Prevalence and trend of neural tube defects in five counties in Shanxi province of Northern China,2000 to 2014.Birth Defects Res A Clin Mol Teratol,2016,106:267-274.
3 Berry RJ,Li Z,Erickson JD,et al.Prevention of neural-tube defects with folic acid in China.China-U.S.Collaborative Project for Neural Tube Defect Prevention.N Engl J Med,1999,341:1485-1490.
4 卫生部.增补叶酸预防神经管缺陷项目管理方案.中国生育健康杂志,2009,20:198-199.
5 Preissler S,Ron D.Early Events in the Endoplasmic Reticulum Unfolded Protein Response.Cold Spring Harb Perspect Biol,2018.
6 李帅峰,胡林,汪加兴,等.线粒体未折叠蛋白反应的研究进展.中国畜牧兽医,2015:1787-1792.
7 Koike N,Hatano Y,Ushimaru T.Heat shock transcriptional factor mediates mitochondrial unfolded protein response.Curr Genet,2018,64:907-917.
8 Pickles S,Vigie P,Youle RJ.Mitophagy and Quality Control Mechanisms in Mitochondrial Maintenance.Curr Biol,2018,28:R170-R185.
9 Zhao Q,Wang J,Levichkin IV,et al.A mitochondrial specific stress response in mammalian cells.EMBO J,2002,21:4411-4419.
10 Lu M,Lawrence DA,Marsters S,et al.Opposing unfolded-protein-response signals converge ondeath receptor 5 to control apoptosis.Science,2014,345:98-101.
11 赵运英,王頔,袁凡,等.酿酒酵母细胞中内质网应激与未折叠蛋白反应的研究进展.微生物学杂志,2017:98-106.
12 Grassi D,Howard S,Zhou M,et al.Identification of a highly neurotoxic alpha-synuclein species inducing mitochondrial damage and mitophagy in Parkinson′s disease.Proc Natl Acad Sci U S A,2018,115:E2634-e2643.
13 Shpilka T,Haynes CM.The mitochondrial UPR:mechanisms,physiological functions and implications in ageing.Nat Rev Mol Cell Biol,2018,19:109-120.
14 马俊香,陈丽,郭彩霞,等.热休克蛋白10与锰致神经细胞凋亡关系的研究.山西医科大学学报,2014:683-687.
15 张媛媛,陈丽,马俊香,等.miR-138-5p在锰致SH-SY5Y细胞自噬中的作用.环境与职业医学,2018:60-65.
16 Berendzen KM,Durieux J,Shao LW,et al.Neuroendocrine Coordination of Mitochondrial Stress Signaling and Proteostasis.Cell,2016,166:1553-1563 e1510.
17 Song D,Ma J,Chen L,et al.FOXO3 promoted mitophagy via nuclear retention induced by manganese chloride in SH-SY5Y cells.Metallomics,2017,9:1251-1259.
18 刘菊芬,靳蕾,任爱国.环境锰暴露对妊娠结局及后代发育的影响.中国生育健康杂志,2012:475-477.
19 Liu J,Jin L,Zhang L,et al.Placental concentrations of manganese and the risk of fetal neural tube defects.J Trace Elem Med Biol,2013,27:322-325.
20 Omori H,Otsu M,Suzuki A,et al.Effects of heat shock on survival,proliferation and differentiation of mouse neural stem cells.Neurosci Res,2014,79:13-21.
21 Buckiova D,Kubinova L,Soukup A,et al.Hyperthermia in the chick embryo:HSP and possible mechanisms of developmental defects.Int J Dev Biol,1998,42:737-740.
22 Kerr SM,Parker SE,Mitchell AA,et al.Periconceptional maternal fever,folic acid intake,and the risk for neural tube defects.Ann Epidemiol,2017,27:777-782.e771.
23 Papaconstantinou AD,Brown KM,Noren BT,et al.Mercury,cadmium,and arsenite enhance heat shock protein synthesis in chick embryos prior to embryotoxicity.Birth Defects Res B Dev Reprod Toxicol,2003,68:456-464.
24 Hunter ES,3rd,Dix DJ.Heat shock proteins Hsp70-1 and Hsp70-3 Are necessary and sufficient to prevent arsenite-induced dysmorphology in mouse embryos.Mol Reprod Dev,2001,59:285-293.
25 Yang P,Reece EA,Wang F,et al.Decoding the oxidative stress hypothesis in diabetic embryopathy through proapoptotic kinase signaling.Am J Obstet Gynecol,2015,212:569-579.
26 Gabbay-Benziv R,Reece EA,Wang F,et al.Birth defects in pregestational diabetes:Defect range,glycemic threshold and pathogenesis.World J Diabetes,2015,6:481-488.
27 Gu H,Yu JW,Dong DY,et al.High Glucose-Repressed CITED2 Expression Through miR-200b Triggers the Unfolded Protein Response and Endoplasmic Reticulum Stress.Diabetes,2016,65:149-163.
28 Wang F,Weng H,Quon MJ,et al.Dominant negative FADD dissipates the proapoptotic signalosome of the unfolded protein response in diabetic embryopathy.Am J Physiol Endocrinol Metab,2015,309:E861-873.
29 Steegers-Theunissen RP,Boers GH,Trijbels FJ,et al.Neural-tube defects and derangement of homocysteine metabolism.N Engl J Med,1991,324:199-200.
30 Kobus-Bianchini K,Bourckhardt GF,Ammar D,et al.Homocysteine-induced changes in cellproliferation and differentiation in the chick embryo spinal cord:implications for mechanisms of neural tube defects (NTD).Reprod Toxicol,2017,69:167-173.
31 Tripathi M,Zhang CW,Singh BK,et al.Hyperhomocysteinemia causes ER stress and impaired autophagy that is reversed by Vitamin B supplementation.Cell Death Dis,2016,7:e2513.
32 Greene ND,Leung KY,Copp AJ.Inositol,neural tube closure and the prevention of neural tube defects.Birth Defects Res,2017,109:68-80.
33 Greene ND,Leung KY,Gay V,et al.Inositol for the prevention of neural tube defects:a pilot randomised controlled trial.Br J Nutr,2016,115:974-983.
34 Dell′Edera D,Sarlo F,Allegretti A,et al.Prevention of neural tube defects and maternal gestational diabetes through the inositol supplementation:preliminary results.Eur Rev Med Pharmacol Sci,2017,21:3305-3311.
35 Gross SM,Rotwein P.Akt signaling dynamics in individual cells.J Cell Sci,2015,128:2509-2519.
36 Crowder RJ,Freeman RS.Glycogen synthase kinase-3 beta activity is critical for neuronal death caused by inhibiting phosphatidylinositol 3-kinase or Akt but not for death caused by nerve growth factor withdrawal.J Biol Chem,2000,275:34266-34271.
37 Garlena RA,Lennox AL,Baker LR,et al.The receptor tyrosine kinase Pvr promotes tissue closure by coordinating corpse removal and epidermal zippering.Development,2015,142:3403-3415.
38 Torroba B,Herrera A,Menendez A,et al.PI3K regulates intraepithelial cell positioning through Rho GTP-ases in the developing neural tube.Dev Biol,2018,436:42-54.
39 Pickett EA,Olsen GS,Tallquist MD.Disruption of PDGFRalpha-initiated PI3K activation and migration of somite derivatives leads to spina bifida.Development,2008,135:589-598.
40 Wang B,Zhang Y,Dong H,et al.Loss of Tctn3 causes neuronal apoptosis and neural tube defects in mice.Cell Death Dis,2018,9:520.
41 Wilson NR,Olm-Shipman AJ,Acevedo DS,et al.SPECC1L deficiency results in increased adherens junction stability and reduced cranial neural crest cell delamination.Sci Rep,2016,6:17735.
42 De Castro SCP,Hirst CS,Savery D,et al.Neural tube closure depends on expression of Grainyhead-like 3 in multiple tissues.Dev Biol,2018,435:130-137.
43 Pyrgaki C,Liu A,Niswander L.Grainyhead-like 2 regulates neural tube closure and adhesion molecule expression during neural fold fusion.Dev Biol,2011,353:38-49.
44 Li XT,Liang Z,Wang TT,et al.Brain-derived Neurotrophic Factor Promotes Growth of Neurons and Neural Stem Cells Possibly by Triggering the Phosphoinositide 3-Kinase/ AKT/Glycogen Synthase Kinase-3beta/beta-catenin Pathway.CNS Neurol Disord Drug Targets,2017,16:828-836.
45 Zhang Q,Shen M,Ding M,et al.The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway.Toxicol Appl Pharmacol,2011,252:62-72.
46 Wang L,Yang HJ,Xia YY,et al.Insulin-like growth factor 1 protects human neuroblastoma cells SH-EP1 against MPP+-induced apoptosis by AKT/GSK-3beta/JNK signaling.Apoptosis,2010,15:1470-1479.