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RETRACTED ARTICLE

Long noncoding RNA HAGLROS regulates apoptosis and autophagy in Parkinson's disease via regulating miR-100/ATG10 axis and PI3K/Akt/mTOR pathway activation.
Artif Cells Nanomed Biotechnol. 2019 Dec; 47(1):2764-2774.AC

Abstract

Parkinson's disease (PD) is a common age-related neurodegenerative disease resulted from the progressive degeneration of dopaminergic neurons in the pars compacta region of substantia nigra. The goal of this study was to investigate the effects and mechanisms of long noncoding RNA (lncRNA) HAGLROS on the apoptosis and autophagy in PD. The MPTP-induced PD mouse model and MPP+-intoxicated SH-SY5Y cell model were established, and the expression levels of HAGLROS and miR-100 were determined. Subsequently, the effects of suppression of HAGLROS on apoptosis and autophagy in MPTP-induced PD mouse model and in MPP+-intoxicated SH-SY5Y cells were investigated. In addition, the association between HAGLROS and miR-100 as well as HAGLROS and activation of phosphoinositide-3 kinase/protein kinase-B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in MPP+-intoxicated SH-SY5Y cells was explored. HAGLROS was increasingly expressed in MPTP-induced PD mouse model and MPP+-intoxicated SH-SY5Y cells and suppression of HAGLRO decreased apoptosis and autophagy in both in vivo and in vitro PD models. Further in vitro studies showed that HAGLRO negatively regulated miR-100 expression, and HAGLROS regulated apoptosis and autophagy of MPP+-intoxicated SH-SY5Y cells through sponging miR-100. Moreover, ATG10 was identified as a target of miR-100. Besides, suppression of HAGLROS alleviated MPP+-intoxicated SH-SY5Y cell injury by activating PI3K/AKT/mTOR pathway. Our findings reveal that upregulation of HAGLROS may contribute to the development of PD via inhibiting apoptosis and autophagy, which may be achieved by regulating miR-100/ATG10 axis and PI3K/AKT/mTOR pathway activation.

Authors+Show Affiliations

a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.b Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.

Pub Type(s)

Journal Article
Retracted Publication

Language

eng

PubMed ID

31298038

Citation

Peng, Tao, et al. "Long Noncoding RNA HAGLROS Regulates Apoptosis and Autophagy in Parkinson's Disease Via Regulating miR-100/ATG10 Axis and PI3K/Akt/mTOR Pathway Activation." Artificial Cells, Nanomedicine, and Biotechnology, vol. 47, no. 1, 2019, pp. 2764-2774.
Peng T, Liu X, Wang J, et al. Long noncoding RNA HAGLROS regulates apoptosis and autophagy in Parkinson's disease via regulating miR-100/ATG10 axis and PI3K/Akt/mTOR pathway activation. Artif Cells Nanomed Biotechnol. 2019;47(1):2764-2774.
Peng, T., Liu, X., Wang, J., Liu, Y., Fu, Z., Ma, X., Li, J., Sun, G., Ji, Y., Lu, J., Wan, W., & Lu, H. (2019). Long noncoding RNA HAGLROS regulates apoptosis and autophagy in Parkinson's disease via regulating miR-100/ATG10 axis and PI3K/Akt/mTOR pathway activation. Artificial Cells, Nanomedicine, and Biotechnology, 47(1), 2764-2774. https://doi.org/10.1080/21691401.2019.1636805
Peng T, et al. Long Noncoding RNA HAGLROS Regulates Apoptosis and Autophagy in Parkinson's Disease Via Regulating miR-100/ATG10 Axis and PI3K/Akt/mTOR Pathway Activation. Artif Cells Nanomed Biotechnol. 2019;47(1):2764-2774. PubMed PMID: 31298038.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Long noncoding RNA HAGLROS regulates apoptosis and autophagy in Parkinson's disease via regulating miR-100/ATG10 axis and PI3K/Akt/mTOR pathway activation. AU - Peng,Tao, AU - Liu,Xiaoyan, AU - Wang,Jingtao, AU - Liu,Yu, AU - Fu,Zhenqiang, AU - Ma,Xingrong, AU - Li,Junmin, AU - Sun,Guifang, AU - Ji,Yangfei, AU - Lu,Jingjing, AU - Wan,Wencui, AU - Lu,Hong, PY - 2019/7/13/entrez PY - 2019/7/13/pubmed PY - 2019/12/18/medline KW - ATG10 phosphoinositide-3 kinase/protein kinase-B/mammalian target of rapamycin pathway KW - HAGLROS KW - Parkinson’s disease KW - miR-100 SP - 2764 EP - 2774 JF - Artificial cells, nanomedicine, and biotechnology JO - Artif Cells Nanomed Biotechnol VL - 47 IS - 1 N2 - Parkinson's disease (PD) is a common age-related neurodegenerative disease resulted from the progressive degeneration of dopaminergic neurons in the pars compacta region of substantia nigra. The goal of this study was to investigate the effects and mechanisms of long noncoding RNA (lncRNA) HAGLROS on the apoptosis and autophagy in PD. The MPTP-induced PD mouse model and MPP+-intoxicated SH-SY5Y cell model were established, and the expression levels of HAGLROS and miR-100 were determined. Subsequently, the effects of suppression of HAGLROS on apoptosis and autophagy in MPTP-induced PD mouse model and in MPP+-intoxicated SH-SY5Y cells were investigated. In addition, the association between HAGLROS and miR-100 as well as HAGLROS and activation of phosphoinositide-3 kinase/protein kinase-B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in MPP+-intoxicated SH-SY5Y cells was explored. HAGLROS was increasingly expressed in MPTP-induced PD mouse model and MPP+-intoxicated SH-SY5Y cells and suppression of HAGLRO decreased apoptosis and autophagy in both in vivo and in vitro PD models. Further in vitro studies showed that HAGLRO negatively regulated miR-100 expression, and HAGLROS regulated apoptosis and autophagy of MPP+-intoxicated SH-SY5Y cells through sponging miR-100. Moreover, ATG10 was identified as a target of miR-100. Besides, suppression of HAGLROS alleviated MPP+-intoxicated SH-SY5Y cell injury by activating PI3K/AKT/mTOR pathway. Our findings reveal that upregulation of HAGLROS may contribute to the development of PD via inhibiting apoptosis and autophagy, which may be achieved by regulating miR-100/ATG10 axis and PI3K/AKT/mTOR pathway activation. SN - 2169-141X UR - https://www.unboundmedicine.com/medline/citation/31298038/Long_noncoding_RNA_HAGLROS_regulates_apoptosis_and_autophagy_in_Parkinson's_disease_via_regulating_miR_100/ATG10_axis_and_PI3K/Akt/mTOR_pathway_activation_ L2 - https://www.tandfonline.com/doi/full/10.1080/21691401.2019.1636805 DB - PRIME DP - Unbound Medicine ER -