Silencing of miR ‐497‐5p inhibits cell apoptosis and promotes autophagy in Parkinson's disease by upregulation of FGF2

2021 ◽  
Author(s):  
Wenjie Zhu ◽  
Hui Zhang ◽  
Jun Gao ◽  
Yun Xu
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Apoptosis

scholarly journals LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson’s Disease through Activating α-Synuclein Expression

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xiaonan Xu ◽  
Chengle Zhuang ◽  
Zimu Wu ◽  
Hongyan Qiu ◽  
Haixia Feng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Long Intergenic Noncoding Rna ◽  
Novel Target ◽  
Underlying Mechanisms

Long intergenic noncoding RNA-p21 (lincRNA-p21) has been reported to be increased in Parkinson’s disease (PD). However, the function and underlying mechanisms of lincRNA-p21 remain not clear. In order to explore the role of lincRNA-p21 in PD, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce in vivo PD model (C57BL/6 mice) and utilized N-methyl-4-phenylpyridinium (MPP+) to create in vitro PD model (SH-SY5Y cells). Results showed that the expression level of lincRNA-p21 was increased significantly in PD models. High abundance of lincRNA-p21 inhibited viability and promoted apoptosis markedly in SH-SY5Y cells treated with MPP+. Mechanistically, further experiments demonstrated that upregulation of lincRNA-p21 could sponge miR-1277-5p and indirectly increase the expression of α-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells. In short, our study illustrated that lincRNA-p21/miR-1277-5p axis regulated viability and apoptosis in SH-SY5Y cells treated with MPP+ via targeting α-synuclein. LincRNA-p21 might be a novel target for PD.

scholarly journals CircSNCA downregulation by pramipexole treatment mediates cell apoptosis and autophagy in Parkinson’s disease by targeting miR-7

Aging ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 1281-1293 ◽  
Author(s):  
Qiuling Sang ◽  
Xiaoyang Liu ◽  
Libo Wang ◽  
Ling Qi ◽  
Wenping Sun ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Apoptosis

scholarly journals Let‑7b‑5p promotes cell apoptosis in Parkinson's disease by targeting HMGA2

2021 ◽  
Vol 24 (5) ◽  
Author(s):  
Yujing Huang ◽  
Ying Liu ◽  
Jing Huang ◽  
Lu Gao ◽  
Zhenggang Wu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Apoptosis

scholarly journals ROCK1 induces dopaminergic nerve cell apoptosis via the activation of Drp1-mediated aberrant mitochondrial fission in Parkinson’s disease

2019 ◽  
Vol 51 (10) ◽  
pp. 1-13 ◽  
Author(s):  
Qian Zhang ◽  
Changpeng Hu ◽  
Jingbin Huang ◽  
Wuyi Liu ◽  
Wenjing Lai ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nerve Cell ◽  
Cell Apoptosis ◽  
Regulatory Mechanism ◽  
Cell Model ◽  
Mitochondrial Fission ◽  
Nerve Cells ◽  
Pathologic Basis

Abstract Dopamine deficiency is mainly caused by apoptosis of dopaminergic nerve cells in the substantia nigra of the midbrain and the striatum and is an important pathologic basis of Parkinson’s disease (PD). Recent research has shown that dynamin-related protein 1 (Drp1)-mediated aberrant mitochondrial fission plays a crucial role in dopaminergic nerve cell apoptosis. However, the upstream regulatory mechanism remains unclear. Our study showed that Drp1 knockdown inhibited aberrant mitochondrial fission and apoptosis. Importantly, we found that ROCK1 was activated in an MPP+-induced PD cell model and that ROCK1 knockdown and the specific ROCK1 activation inhibitor Y-27632 blocked Drp1-mediated aberrant mitochondrial fission and apoptosis of dopaminergic nerve cells by suppressing Drp1 dephosphorylation/activation. Our in vivo study confirmed that Y-27632 significantly improved symptoms in a PD mouse model by inhibiting Drp1-mediated aberrant mitochondrial fission and apoptosis. Collectively, our findings suggest an important molecular mechanism of PD pathogenesis involving ROCK1-regulated dopaminergic nerve cell apoptosis via the activation of Drp1-induced aberrant mitochondrial fission.

LncRNA MALAT1 targeting miR‐124‐3p regulates DAPK1 expression contributes to cell apoptosis in Parkinson's Disease

2020 ◽  
Vol 121 (12) ◽  
pp. 4838-4848 ◽  
Author(s):  
Yi Lu ◽  
Zhongying Gong ◽  
Xiaojie Jin ◽  
Peng Zhao ◽  
Yuting Zhang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Apoptosis ◽  
Lncrna Malat1

scholarly journals Protective Effect of Compound Formula Rehmannia against Neurotoxicity and Apoptosis Induced by α-Syn in In Vivo and In Vitro Models of Parkinson’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Long Teng ◽  
Minchun Yang ◽  
Xiaoqing Jin ◽  
Lu Qian ◽  
Weijia Yang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
In Vitro Models ◽  
Western Blot Assay ◽  
Rotation Numbers

The present study aimed to investigate the protective effect of compound formula Rehmannia (CFR) against the development of Parkinson’s disease (PD). After the in vivo and in vitro models of PD were established with overexpression α-syn induced, CFR was administrated into the PD model rats for 6 weeks or SK-N-SH cells with coincubation for 48 h. Apomorphine-induced rotation test, CCK8 assay, TUNEL assay, immunofluorescence staining, and western blot assay were performed to evaluate the behavioral changes, cell viability, cell apoptosis, α-syn, GSK-3β, P-GSK-3β (Ser9), P-GSK-3β (Tyr216), and β-catenin expression in PD rats or SK-N-SH cells. PD rat behavior results showed that the rotation numbers were significantly decreased in the CFR treatment group comparing with the AAV-α-syn PD model group. The cell viability suppressed by H2O2 and α-syn in SK-N-SH model cells was also significantly improved with CFR administration. Cell apoptosis and α-syn overexpression observed in PD rats and SK-N-SH cells were also inhibited by CFR treatment. Furthermore, the protein expression of α-syn, GSK-3β, P-GSK-3β (Ser9), P-GSK-3β (Tyr216), and β-catenin in in vivo and in vitro was also significantly regulated by CFR. The present study suggested that CFR may be considered as a potential neuroprotective agent against PD, and this application will require further investigation.

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