热休克转录因子1及热休克蛋白70与阿尔茨海默病的关系
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摘要
阿尔茨海默病(AD)是痴呆中最常见的一种神经退行性疾病,越来越多的证据表明,AD是一种"蛋白质错误折叠障碍性疾病",具有蛋白质错误折叠、易聚集和成熟神经系统中选择性细胞丢失的共同特征。热休克蛋白(HSP)是细胞中一组重要的分子伴侣蛋白,它参与了辅助蛋白质合成、折叠、定位及转运等过程,并且在协助蛋白质水解、预防蛋白质错误折叠和聚集方面具有重要的作用,有研究证实HSP与AD存在密切的联系。HSP70是HSP中最保守、最丰富的一个伴侣蛋白。HSP70不但可抑制β-淀粉样肽(Aβ)相关的毒性作用,也在tau蛋白的聚积或降解中发挥重要作用。这些研究结果提示HSP70有可能成为AD治疗的新靶点,本文对HSP70及其上游调控因子HSF1与AD的关系作一综述。
引文
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[25]PLYTE S E,HUGHES K,NIKOLAKAKI E,et al. Glycogen synthase kinase-3:functions in oncogenesis and development[J]. Biochimica et biophysica acta,1992,1114(2-3):147-162.
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[27]CHENG H,XIA B,SU C,et al. PI3K/Akt signaling pathway and Hsp70 activate in hippocampus of rats with chronic manganese sulfate exposure[J]. Journal of Trace Elements in Medicine and Biology,2018,50(12):332-338.
[28]FANG X,JIANG Y,FENG L,et al. Blockade of PI3K/AKT pathway enhances sensitivity of Raji cells to chemotherapy through down-regulation of HSP70[J]. Cancer Cell International,2013,13(1):48-55.
[29]MA K,QIAN Y. Alpha 7 nicotinic acetylcholine receptor and its effects on Alzheimer's disease[J]. Neuropeptides,2019,73(2):96-106.
[30]KAWAMATA J,SHIMOHAMA S. Stimulating nicotinic receptors trigger multiple pathways attenuating cytotoxicity in models of Alzheimer's and Parkinson's diseases[J].Journal of Alzheimers Disease Jad,2011,24(Suppl 2):95-109.
[31]YU W,MECHAWAR N,KRANTIC S,et al.α7 Nicotinic receptor activation reducesβ-amyloid-induced apoptosis by inhibiting caspase-independent death through phosphatidylinositol 3-kinase signaling[J]. Journal of Neurochemistry,2011,119(4):848-858.
[32]HUANG X,CHENG Z,SU Q,et al. Neuroprotection by nicotine against colchicine-induced apoptosis is mediated by PI3-Kinase-Akt pathways[J]. International Journal of Neuroscience,2012,122(6):324-332.
[33]ZHENKUI REN M Y Z G. Astrocyticα7 nicotinic receptor activation inhibits amyloid-βaggregation by upregulating endogenousαB-crystallin through the PI3K/Akt signaling pathway[J]. 2019,16(1):39-48.
[2] SELKOE D J,HARDY J. The amyloid hypothesis of Alzheimer's disease at 25 years[J]. EMBO Mol Med,2016,8(6):595-608.
[3]CHEIGNON C,TOMAS M,BONNEFONT-ROUSSELOT D,et al. Oxidative stress and the amyloid beta peptide in Alzheimer’s disease[J]. Redox Biology,2018,14(3):450-464.
[4]YAN M H,WANG X,ZHU X. Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease[J]. Free Radical Biology and Medicine,2013,62(11):90-101.
[5]CAMPANELLA C,PACE A,CARUSO BAVISOTTO C,et al. Heat shock proteins in Alzheimer’s disease:role and targeting[J]. International Journal of Molecular Sciences,2018,19(9):2603-2625.
[6]MURPHY M E. The HSP70 family and cancer[J]. Carcinogenesis,2013,34(6):1181-1188.
[7] MERIIN A B,NARAYANAN A,MENG L,et al.Hsp70-Bag3 complex is a hub for proteotoxicity-induced signaling that controls protein aggregation[J]. Proceedings of the National Academy of Sciences,2018,115(30):7043-7052.
[8]JORES T,LAWATSCHECK J,BEKE V,et al. Cytosolic Hsp70 and Hsp40 chaperones enable the biogenesis of mitochondrialβ-barrel proteins[J]. The Journal of Cell Biology,2018,217(9):3091-3108.
[9]SUN Y,ZHANG J R,CHEN S. Suppression of Alzheimer's disease-related phenotypes by the heat shock protein70 inducer,geranylgeranylacetone,in APP/PS1 transgenic mice via the ERK/p38 MAPK signaling pathway[J].Exp Ther Med,2017,14(6):5267-5274.
[10]HOSHINO T,MURAO N,NAMBA T,et al. Suppression of Alzheimer's disease-related phenotypes by expression of heat shock protein 70 in mice[J]. Journal of Neuroscience,2011,31(14):5225-5234.
[11]MAITI P,MANNA J,VELERI S,et al. Molecular chaperone dysfunction in neurodegenerative diseases and effects of curcumin[J]. Bio Med Research International,2014,2014(10):1-14.
[12]KOREN J,JINWAL U K,LEE D C,et al. Chaperone signaling complexes in Alzheimer's disease[J]. Journal of Cellular and Molecular Medicine,2009,13(4):619-630.
[13]FERNANDEZ-FUNEZ P, SANCHEZ-GARCIA J, de MENA L, et al. Holdase activity of secreted Hsp70masks amyloid-β42 neurotoxicity in Drosophila[J]. Proceedings of the National Academy of Sciences,2016,113(35):5212-5221.
[14]GOMEZ-PASTOR R,BURCHFIEL E T,THIELE D J.Regulation of heat shock transcription factors and their roles in physiology and disease[J]. Nature Reviews Molecular Cell Biology,2017,19(1):4-19.
[15]VERMA P,PFISTER J A,MALLICK S,et al. HSF1protects neurons through a novel trimerization-and hspindependent mechanism[J]. Journal of Neuroscience,2014,34(5):1599-1612.
[16]HOOPER P L,DURHAM H D,TOROK Z,et al. The central role of heat shock factor 1 in synaptic fidelity and memory consolidation[J]. Cell Stress and Chaperones,2016,21(5):745-753.
[17]GOMEZ-PASTOR R,BURCHFIEL E T,THIELE D J.Regulation of heat shock transcription factors and their roles in physiology and disease[J]. Nature Reviews Molecular Cell Biology,2017,19(1):4-19.
[18]PIERCE A,PODLUTSKAYA N,HALLORAN J J,et al.Over-expression of heat shock factor 1 phenocopies the effect of chronic inhibition of TOR by rapamycin and is sufficient to ameliorate Alzheimer's-like deficits in mice modeling the disease[J]. Journal of Neurochemistry,2013,124(6):880-893.
[19]JIANG Y,WANG X,CAO X,et al. Increased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease[J].Brain Research,2013,1519(6):105-111.
[20]ZHANG B,HE P,LU Y,et al. HSF1 Relieves Amyloid-β-induced cardiomyocytes apoptosis[J]. Cell Biochemistry and Biophysics,2015,72(2):579-587.
[21]CHOW A M,TANG D W F,HANIF A,et al. Localization of heat shock proteins in cerebral cortical cultures following induction by celastrol[J]. Cell Stress and Chaperones,2014,19(6):845-851.
[22]SHARMA S,MISHRA R,WALKER B L,et al. Celastrol,an oral heat shock activator,ameliorates multiple animal disease models of cell death[J]. Cell Stress and Chaperones,2015,20(1):185-201.
[23]PARIS D,GANEY N J,LAPORTE V,et al. Reduction of beta-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer's disease[J]. J Neuroinflammation,2010,7:17.
[24]YU H,KOH S. The role of PI3K/AKT pathway and its therapeutic possibility in Alzheimer's disease[J]. Hanyang Medical Reviews,2017,37(1):18-24.
[25]PLYTE S E,HUGHES K,NIKOLAKAKI E,et al. Glycogen synthase kinase-3:functions in oncogenesis and development[J]. Biochimica et biophysica acta,1992,1114(2-3):147-162.
[26]RAFIEE P,THERIOT M E,NELSON V M,et al. Human esophageal microvascular endothelial cells respond to acidic p H stress by PI3K/AKT and p38 MAPK-regulated induction of Hsp70 and Hsp27[J]. Am J Physiol Cell Physiol,2006,291(5):931-945.
[27]CHENG H,XIA B,SU C,et al. PI3K/Akt signaling pathway and Hsp70 activate in hippocampus of rats with chronic manganese sulfate exposure[J]. Journal of Trace Elements in Medicine and Biology,2018,50(12):332-338.
[28]FANG X,JIANG Y,FENG L,et al. Blockade of PI3K/AKT pathway enhances sensitivity of Raji cells to chemotherapy through down-regulation of HSP70[J]. Cancer Cell International,2013,13(1):48-55.
[29]MA K,QIAN Y. Alpha 7 nicotinic acetylcholine receptor and its effects on Alzheimer's disease[J]. Neuropeptides,2019,73(2):96-106.
[30]KAWAMATA J,SHIMOHAMA S. Stimulating nicotinic receptors trigger multiple pathways attenuating cytotoxicity in models of Alzheimer's and Parkinson's diseases[J].Journal of Alzheimers Disease Jad,2011,24(Suppl 2):95-109.
[31]YU W,MECHAWAR N,KRANTIC S,et al.α7 Nicotinic receptor activation reducesβ-amyloid-induced apoptosis by inhibiting caspase-independent death through phosphatidylinositol 3-kinase signaling[J]. Journal of Neurochemistry,2011,119(4):848-858.
[32]HUANG X,CHENG Z,SU Q,et al. Neuroprotection by nicotine against colchicine-induced apoptosis is mediated by PI3-Kinase-Akt pathways[J]. International Journal of Neuroscience,2012,122(6):324-332.
[33]ZHENKUI REN M Y Z G. Astrocyticα7 nicotinic receptor activation inhibits amyloid-βaggregation by upregulating endogenousαB-crystallin through the PI3K/Akt signaling pathway[J]. 2019,16(1):39-48.