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Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells.
Neurotox Res. 2017 Oct; 32(3):351-361.NR

Abstract

Autophagy is an evolutionary conserved catabolic process that ensures continuous removal of damaged cell organelles and long-lived protein aggregates to maintain cellular homeostasis. Although autophagy has been implicated in amyloid-β (Aβ) production and deposition, its role in pathogenesis of Alzheimer's disease remains elusive. Thus, the present study was undertaken to assess the cytoprotective and neuroprotective potential of autophagy on Aβ-induced oxidative stress, apoptosis and neurotoxicity in human neuroblastoma SH-SY5Y cells. The treatment of Aβ1-42 impaired the cell growth and redox balance, and induced apoptosis and neurotoxicity in SH-SY5Y cells. Next, the treatment of rapamycin (RAP) significantly elevated the expression of autophagy markers such as microtubule-associated protein-1 light chain-3 (LC3), sequestosome-1/p62, Beclin-1, and unc-51-like kinase-1 (ULK1) in SH-SY5Y cells. RAP-induced activation of autophagy notably alleviated the Aβ1-42-induced impairment of redox balance by decreasing the levels of pro-oxidants such as reactive oxygen species, lipid peroxidation and Ca2+ influx, and concurrently increasing the levels of antioxidant enzymes such as superoxide dismutase and catalase. The RAP-induced autophagy also ameliorated Aβ1-42-induced loss of mitochondrial membrane potential and apoptosis. Additionally, the activated autophagy provided significant neuroprotection against Aβ1-42-induced neurotoxicity by elevating the expression of neuronal markers such as synapsin-I, PSD95, NCAM, and CREB. However, 3-methyladenine treatment significantly exacerbated the neurotoxic effects of Aβ1-42. Taken together, our study demonstrated that the activation of autophagy provided possible neuroprotection against Aβ-induced cytotoxicity, oxidative stress, apoptosis, and neurotoxicity in SH-SY5Y neuronal cells.

Authors+Show Affiliations

Department of Biochemistry, University of Allahabad, Allahabad, 211002, India. aks84m@gmail.com.Department of Biomedical Engineering, National Institute of Technology, Raipur, 492010, India.Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213, USA.Department of Biochemistry, Pt. JNM Medical College, Raipur, 492001, India.Department of Biochemistry, University of Allahabad, Allahabad, 211002, India.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28484969

Citation

Singh, Abhishek Kumar, et al. "Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells." Neurotoxicity Research, vol. 32, no. 3, 2017, pp. 351-361.
Singh AK, Bissoyi A, Kashyap MP, et al. Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells. Neurotox Res. 2017;32(3):351-361.
Singh, A. K., Bissoyi, A., Kashyap, M. P., Patra, P. K., & Rizvi, S. I. (2017). Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells. Neurotoxicity Research, 32(3), 351-361. https://doi.org/10.1007/s12640-017-9746-5
Singh AK, et al. Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells. Neurotox Res. 2017;32(3):351-361. PubMed PMID: 28484969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells. AU - Singh,Abhishek Kumar, AU - Bissoyi,Akalabya, AU - Kashyap,Mahendra Pratap, AU - Patra,Pradeep Kumar, AU - Rizvi,Syed Ibrahim, Y1 - 2017/05/08/ PY - 2017/03/06/received PY - 2017/04/21/accepted PY - 2017/04/19/revised PY - 2017/5/10/pubmed PY - 2018/8/7/medline PY - 2017/5/10/entrez KW - 3-Methyladenine KW - Amyloid-beta KW - Autophagy KW - Neuroblastoma SH-SY5Y cells KW - Neuroprotection KW - Oxidative stress KW - Rapamycin SP - 351 EP - 361 JF - Neurotoxicity research JO - Neurotox Res VL - 32 IS - 3 N2 - Autophagy is an evolutionary conserved catabolic process that ensures continuous removal of damaged cell organelles and long-lived protein aggregates to maintain cellular homeostasis. Although autophagy has been implicated in amyloid-β (Aβ) production and deposition, its role in pathogenesis of Alzheimer's disease remains elusive. Thus, the present study was undertaken to assess the cytoprotective and neuroprotective potential of autophagy on Aβ-induced oxidative stress, apoptosis and neurotoxicity in human neuroblastoma SH-SY5Y cells. The treatment of Aβ1-42 impaired the cell growth and redox balance, and induced apoptosis and neurotoxicity in SH-SY5Y cells. Next, the treatment of rapamycin (RAP) significantly elevated the expression of autophagy markers such as microtubule-associated protein-1 light chain-3 (LC3), sequestosome-1/p62, Beclin-1, and unc-51-like kinase-1 (ULK1) in SH-SY5Y cells. RAP-induced activation of autophagy notably alleviated the Aβ1-42-induced impairment of redox balance by decreasing the levels of pro-oxidants such as reactive oxygen species, lipid peroxidation and Ca2+ influx, and concurrently increasing the levels of antioxidant enzymes such as superoxide dismutase and catalase. The RAP-induced autophagy also ameliorated Aβ1-42-induced loss of mitochondrial membrane potential and apoptosis. Additionally, the activated autophagy provided significant neuroprotection against Aβ1-42-induced neurotoxicity by elevating the expression of neuronal markers such as synapsin-I, PSD95, NCAM, and CREB. However, 3-methyladenine treatment significantly exacerbated the neurotoxic effects of Aβ1-42. Taken together, our study demonstrated that the activation of autophagy provided possible neuroprotection against Aβ-induced cytotoxicity, oxidative stress, apoptosis, and neurotoxicity in SH-SY5Y neuronal cells. SN - 1476-3524 UR - https://www.unboundmedicine.com/medline/citation/28484969/Autophagy_Activation_Alleviates_Amyloid_β_Induced_Oxidative_Stress_Apoptosis_and_Neurotoxicity_in_Human_Neuroblastoma_SH_SY5Y_Cells_ L2 - https://dx.doi.org/10.1007/s12640-017-9746-5 DB - PRIME DP - Unbound Medicine ER -