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We began analyzing https://www.nature.com/articles/cddis201373, but it redirected us to https://www.nature.com/articles/cddis201373. The analysis below is for the second page.

Title[redir]:
Influence of microRNA deregulation on chaperone-mediated autophagy and α-synuclein pathology in Parkinson's disease | Cell Death & Disease
Description:
The presence of α-synuclein aggregates in the characteristic Lewy body pathology seen in idiopathic Parkinson’s disease (PD), together with α-synuclein gene mutations in familial PD, places α-synuclein at the center of PD pathogenesis. Decreased levels of the chaperone-mediated autophagy (CMA) proteins LAMP-2A and hsc70 in PD brain samples suggests compromised α-synuclein degradation by CMA may underpin the Lewy body pathology. Decreased CMA protein levels were not secondary to the various pathological changes associated with PD, including mitochondrial respiratory chain dysfunction, increased oxidative stress and proteasomal inhibition. However, decreased hsc70 and LAMP-2A protein levels in PD brains were associated with decreases in their respective mRNA levels. MicroRNA (miRNA) deregulation has been reported in PD brains and we have identified eight miRNAs predicted to regulate LAMP-2A or hsc70 expression that were reported to be increased in PD. Using a luciferase reporter assay in SH-SY5Y cells, four and three of these miRNAs significantly decreased luciferase activity expressed upstream of the lamp-2a and hsc70 3′UTR sequences respectively. We confirmed that transfection of these miRNAs also decreased endogenous LAMP-2A and hsc70 protein levels respectively and resulted in significant α-synuclein accumulation. The analysis of PD brains confirmed that six and two of these miRNAs were significantly increased in substantia nigra compacta and amygdala respectively. These data support the hypothesis that decreased CMA caused by miRNA-induced downregulation of CMA proteins plays an important role in the α-synuclein pathology associated with PD, and opens up a new avenue to investigate PD pathogenesis.

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Keywords {🔍}

levels, αsynuclein, lampa, hsc, mirnas, protein, mrna, cells, article, pubmed, google, scholar, disease, mirna, figure, increased, cas, cell, target, decrease, parkinsons, hsamir, luciferase, cma, predicted, utr, shsyy, supplementary, nature, brain, control, relative, data, decreased, amygdala, actin, microrna, brains, alphasynuclein, snc, concentrations, analysis, autophagy, proteins, samples, degradation, reported, significant, normal, hsamira,

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nature portfolio privacy policy received research funding brain research trust dmem/f12 media supplemented horseradish peroxidase-conjugated anti-mouse regional government bodies biodonostia research institute nature 1997 nature 2010 nature sds-soluble α-synuclein monomer advertising microrna cluster mir-29a/b-1 increased bace1/beta-secretase expression south africa attend scientific meetings 0/ reprints chaperone-mediated autophagy markers endogenous α-synuclein gene wild type alpha-synuclein open bars c-terminal hemagglutinin tag α-synuclein overexpressing cells nonparametric kruskal–wallis test mann–whitney u-test normal sh-sy5y cells luciferase-3′utr lamp-2a constructs overexpressed α-synuclein excluded express endogenous α-synuclein altered alpha-synuclein metabolism intracellular α-synuclein levels α-synuclein monomer levels thermo scientific compromised α-synuclein degradation induce α-synuclein accumulation normal sh-sh5y cells social media α-synuclein accumulation characteristic α-synuclein gene mutations s129 phosphorylated α-synuclein modulate α-synuclein expression endogenous α-synuclein mrna alpha-synuclein locus triplication single-stranded rna molecules α-synuclein aggregates accumulate α-synuclein protein levels significant α-synuclein accumulation increased α-synuclein levels α-synuclein protein relative

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         headline:Influence of microRNA deregulation on chaperone-mediated autophagy and Î±-synuclein pathology in Parkinson's disease
         description:The presence of Î±-synuclein aggregates in the characteristic Lewy body pathology seen in idiopathic Parkinsonâs disease (PD), together with Î±-synuclein gene mutations in familial PD, places Î±-synuclein at the center of PD pathogenesis. Decreased levels of the chaperone-mediated autophagy (CMA) proteins LAMP-2A and hsc70 in PD brain samples suggests compromised Î±-synuclein degradation by CMA may underpin the Lewy body pathology. Decreased CMA protein levels were not secondary to the various pathological changes associated with PD, including mitochondrial respiratory chain dysfunction, increased oxidative stress and proteasomal inhibition. However, decreased hsc70 and LAMP-2A protein levels in PD brains were associated with decreases in their respective mRNA levels. MicroRNA (miRNA) deregulation has been reported in PD brains and we have identified eight miRNAs predicted to regulate LAMP-2A or hsc70 expression that were reported to be increased in PD. Using a luciferase reporter assay in SH-SY5Y cells, four and three of these miRNAs significantly decreased luciferase activity expressed upstream of the lamp-2a and hsc70 3â²UTR sequences respectively. We confirmed that transfection of these miRNAs also decreased endogenous LAMP-2A and hsc70 protein levels respectively and resulted in significant Î±-synuclein accumulation. The analysis of PD brains confirmed that six and two of these miRNAs were significantly increased in substantia nigra compacta and amygdala respectively. These data support the hypothesis that decreased CMA caused by miRNA-induced downregulation of CMA proteins plays an important role in the Î±-synuclein pathology associated with PD, and opens up a new avenue to investigate PD pathogenesis.
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      headline:Influence of microRNA deregulation on chaperone-mediated autophagy and Î±-synuclein pathology in Parkinson's disease
      description:The presence of Î±-synuclein aggregates in the characteristic Lewy body pathology seen in idiopathic Parkinsonâs disease (PD), together with Î±-synuclein gene mutations in familial PD, places Î±-synuclein at the center of PD pathogenesis. Decreased levels of the chaperone-mediated autophagy (CMA) proteins LAMP-2A and hsc70 in PD brain samples suggests compromised Î±-synuclein degradation by CMA may underpin the Lewy body pathology. Decreased CMA protein levels were not secondary to the various pathological changes associated with PD, including mitochondrial respiratory chain dysfunction, increased oxidative stress and proteasomal inhibition. However, decreased hsc70 and LAMP-2A protein levels in PD brains were associated with decreases in their respective mRNA levels. MicroRNA (miRNA) deregulation has been reported in PD brains and we have identified eight miRNAs predicted to regulate LAMP-2A or hsc70 expression that were reported to be increased in PD. Using a luciferase reporter assay in SH-SY5Y cells, four and three of these miRNAs significantly decreased luciferase activity expressed upstream of the lamp-2a and hsc70 3â²UTR sequences respectively. We confirmed that transfection of these miRNAs also decreased endogenous LAMP-2A and hsc70 protein levels respectively and resulted in significant Î±-synuclein accumulation. The analysis of PD brains confirmed that six and two of these miRNAs were significantly increased in substantia nigra compacta and amygdala respectively. These data support the hypothesis that decreased CMA caused by miRNA-induced downregulation of CMA proteins plays an important role in the Î±-synuclein pathology associated with PD, and opens up a new avenue to investigate PD pathogenesis.
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