RETRACTED ARTICLE: Long noncoding RNA HAGLROS regulates apoptosis and autophagy in Parkinson’s disease via regulating miR-100/ATG10 axis and PI3K/Akt/mTOR pathway activation

Peng, Tao; Liu, Xiaoyan; Wang, Jingtao; Liu, Yü; Fu, Zhenqiang; Ma, Xiaoli; Li, Junmin; Sun, Guifang; Ji, Yangfei; Lu, Jingjing; Wan, Wencui; Lü, Hong

doi:10.1080/21691401.2019.1636805

Cited by 58 publications

(26 citation statements)

References 45 publications

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“…The report also explicated that miRNAs protected cell from damage via regulating the above two kinds of pathways in neurodegenerative diseases [43,44]. For instance, up-regulating miR-100 expression evoked the simulation of PI3K/AKT/mTOR pathway to decrease the incidence of PD [43]. Down-regulating miR-214 expression induced the simulation of Wnt/b-catenin pathway to decline the rate of HD [44].…”

Section: Discussionmentioning

confidence: 93%

“…Research also explained that the blockage of Wnt/ b-catenin pathway was partially activated to protect nerve cells in PD and AD [41,42]. The report also explicated that miRNAs protected cell from damage via regulating the above two kinds of pathways in neurodegenerative diseases [43,44]. For instance, up-regulating miR-100 expression evoked the simulation of PI3K/AKT/mTOR pathway to decrease the incidence of PD [43].…”

Section: Discussionmentioning

confidence: 95%

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Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α

Yang

Kong

2020

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Although dexmedetomidine (Dex) has a significant neuroprotective effect in various nerve-damage models, the exact mechanism of which Dex protects cells from oxidative damage is not fully clear. This article recommended the protective effect of Dex on oxidative damage in PC12 cells. Methods: The PC12 cells were incubated by hydrogen peroxide (H 2 O 2) for 24 h and pre-treated by Dex for 30 min. Cell viability, apoptosis, HIF-1a expression and ROS level were detected by CCK-8, apoptosis assay, Western blot and ROS assay, respectively. The miR-199a expression was tested by qRT-PCR. Targeting relationship between miR-199a and HIF-1a was performed by dual luciferase activity assay. The activation of PI3K/AKT/mTOR and Wnt/b-catenin pathways was tested by western blot. Results: Dex attenuated H 2 O 2-induced oxidative damage, including the decline of cell viability, the raise of apoptosis and the generation of ROS in PC12 cells by down-regulating miR-199a expression. Moreover, Dex up-regulated HIF-1a expression via decreasing miR-199a level in PC12 cells and miR-199a targeted the 3 0-UTR of HIF-1a. In addition, Dex activated PI3K/AKT/mTOR and Wnt/b-catenin pathways by declining miR-199a level. Conclusions: This article illustrated the protective effect of Dex on oxidative damage in PC12 cells. Furthermore, Dex prevented PC12 cells from oxidative injury through the regulation of miR-199a/ HIF-1a.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 95%

Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α

Yang

Kong

2020

Artificial Cells, Nanomedicine, and Biotechnology

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“…Several natural compounds, such as kaempferol, celastrol, and resveratrol, could enhance autophagy, and thus exert neuroprotective effects in PD models [51][52][53][54][55]. More recently, long noncoding RNA HAGLROS modulated autophagy and apoptosis by controlling PI3K/Akt/mTOR activation and miR-100/ATG10 signaling in PD [56]. In the brain, apelin-13 protected dopaminergic neurons in MPTP-induced PD model mice in vivo, through inhibiting ERS and promoting autophagy [17].…”

Section: Discussionmentioning

confidence: 99%

Apelin-13 Protects Dopaminergic Neurons against Rotenone—Induced Neurotoxicity through the AMPK/mTOR/ULK-1 Mediated Autophagy Activation

Chen

Wang

Chen

et al. 2020

IJMS

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Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Several brain–gut peptides are able to exert neuroprotective effects on the nigrostriatal dopaminergic system. Apelin-13 is a neuropeptide, conveying potential neuroprotective activities. However, whether, and how, apelin-13 could antagonize rotenone-induced neurotoxicity has not yet been elucidated. In the present study, rotenone-treated SH-SY5Y cells and rats were used to clarify whether apelin-13 has protective effects on dopaminergic neurons, both in vivo and in vitro. The results showed that apelin-13 could protect SH-SY5Y cells from rotenone-induced injury and apoptosis. Apelin-13 was able to activate autophagy, and restore rotenone induced autophagy impairment in SH-SY5Y cells, which could be blocked by the autophagy inhibitor 3-Methyladenine. Apelin-13 activated AMPK/mTOR/ULK-1 signaling, AMPKα inhibitor compound C, as well as apelin receptor blockage via siRNA, which could block apelin-13-induced signaling activation, autophagy activation, and protective effects, in rotenone-treated SH-SY5Y cells. These results indicated that apelin-13 exerted neuroprotective properties against rotenone by stimulating AMPK/mTOR/ULK-1 signaling-mediated autophagy via the apelin receptor. We also observed that intracerebroventricular injection of apelin-13 could alleviate nigrostriatal dopaminergic neuron degeneration in rotenone-treated rats. Our findings provide new insights into the mechanism by which apelin-13 might attenuate neurotoxicity in PD.

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“…[46]. Suppression of HAGLRO can also decrease apoptosis and autophagy in both in vivo and in vitro PD models [29].…”

Section: Lncrnas and Apoptosis Of Dopaminergic Neurons In Pdmentioning

confidence: 99%

Role of Long Noncoding RNAs in Parkinson’s Disease: Putative Biomarkers and Therapeutic Targets

Wang

Zhong

et al. 2020

Parkinson's Disease

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Parkinson’s disease (PD) is a neurodegenerative disease characterized by bradykinesia, rigidity, and tremor. Age is the main risk factor. Long noncoding RNAs (lncRNAs) are novel RNA molecules of more than 200 nucleotides in length. They may be involved in the regulation of many pathological processes of PD. PD has a variety of pathophysiological mechanisms, including alpha-synuclein aggregate, mitochondrial dysfunction, oxidative stress, calcium homeostasis, axonal transport, and neuroinflammation. Among these, the impacts of lncRNAs on the pathogenesis and progression of PD need to be highlighted. lncRNAs may serve as putative biomarkers and therapeutic targets for the early diagnosis of PD. This study aimed to investigate the role of lncRNAs in various pathological processes of PD and the specific lncRNAs that might be used as putative diagnostic biomarkers and therapeutic targets of PD.

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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

Cited by 58 publications

References 45 publications

Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α

Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α

Apelin-13 Protects Dopaminergic Neurons against Rotenone—Induced Neurotoxicity through the AMPK/mTOR/ULK-1 Mediated Autophagy Activation

Role of Long Noncoding RNAs in Parkinson’s Disease: Putative Biomarkers and Therapeutic Targets

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