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 LncRNA MALAT1 aggravates MPP-induced neuronal injury by regulating miR-212 in SH-SY5Y cells

RSC Advances ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. 690-698
Author(s):  
Dahua Yuan ◽  
Qun Wang ◽  
Nan Ding ◽  
Pu Du ◽  
Lingmei Peng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disease ◽  
Neuronal Injury ◽  
Lncrna Malat1

Parkinson's disease (PD) is the most common neurodegenerative disease and its incidence is rising.

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.

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