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mice, vpsdn, vps, mitochondrial, knockin, pubmed, daergic, protein, neurons, article, months, heterozygous, snpc, fig, google, scholar, level, caspase, wnt, cas, monthold, disease, activity, mitochondria, aged, mouse, expression, complex, signaling, parkinsons, mutation, park, cell, active, cytosolic, mutant, observed, age, bar, wntβcatenin, dysfunction, central, found, retromer, compared, pathway, nuclear, βcatenin, study, upregulated,

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nature portfolio shu-yu liu & hung-li wang privacy policy open-field behavioral space activating wnt/β-catenin pathway27 wnt/beta-catenin signaling pathway nature anti-phospho-tauser202/thr205 antibody demonstrated anti-phospho-tauser202/thr205 antiserum showed canonical wnt/β-catenin pathway24 advertising wnt/β-catenin signaling cascade wnt/β-catenin signaling pathway exhibit late-onset neurodegeneration dysregulated wnt/β-catenin signaling ethanol solutions wnt/β-catenin neuroprotective signaling late-onset parkinsonian syndromes 5 mg/kg/body weight research groups7 wnt/β-catenin signaling activity social media vps35–vps29–vps26 trimer participates hung-li wang multi-centre clinico-genetic analysis wnt/beta-catenin pathway late-onset parkinsonism syndromes3 releases chromophore p-nitroaniline reprints hypokinesia phenotype displayed l-dopa treatment exerts wnt/β-catenin cascade wnt/β-catenin pathway wnt/β-catenin signaling probe-dependent proximity profiling wnt/β-catenin cascade24 methyl l-dopa performing oligonucleotide-directed mutagenesis loxp-flanked neomycin selection screen neomycin-resistant colonies yu-ting wang vps26–vps29–vps35 trimer nuclear β-catenin exerts nuclear β-catenin promotes late-onset parkinson disease late-onset loss upregulated phospho-tauser202/thr205 level late-onset pd7 anti-complex ii antibody full size image

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• Can we safely target the WNT pathway?
• Mitochondria: a therapeutic target for Parkinson’s disease?

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         headline:(D620N) VPS35 causes the impairment of Wnt/β-catenin signaling cascade and mitochondrial dysfunction in a PARK17 knockin mouse model
         description:Patients with familial type 17 of Parkinson’s disease (PARK17) manifest autosomal dominant pattern and late-onset parkinsonian syndromes. Heterozygous (D620N) mutation of vacuolar protein sorting 35 (VPS35) is genetic cause of PARK17. We prepared heterozygous VPS35D620N/+ knockin mouse, which is an ideal animal model of (D620N) VPS35-induced autosomal dominant PARK17. Late-onset loss of substantia nigra pars compacta (SNpc) dopaminergic (DAergic) neurons and motor deficits of Parkinson’s disease were found in 16-month-old VPS35D620N/+ mice. Normal function of VPS35-containing retromer is needed for activity of Wnt/β-catenin cascade, which participates in protection and survival of SNpc DAergic neurons. It was hypothesized that (D620N) VPS35 mutation causes the malfunction of VPS35 and resulting impaired activity of Wnt/β-catenin pathway. Protein levels of Wnt1 and nuclear β-catenin were reduced in SN of 16-month-old VPS35D620N/+ knockin mice. Downregulated protein expression of survivin, which is a target gene of nuclear β-catenin, and upregulated protein levels of active caspase-8 and active caspase-9 were observed in SN of VPS35D620N/+ mice at age of 16 months. VPS35 is involved in controlling morphology and function of mitochondria. Impaired function of VPS35 caused by (D620N) mutation could lead to abnormal morphology and malfunction of mitochondria. A significant decrease in mitochondrial size and resulting mitochondrial fragmentation was found in tyrosine hydroxylase-positive and neuromelanin-positive SNpc DAergic neurons of 16-month-old VPS35D620N/+ mice. Mitochondrial complex I activity or complex IV activity was reduced in SN of 16-month-old VPS35D620N/+ mice. Increased level of mitochondrial ROS and oxidative stress were found in SN of 16-month-old VPS35D620N/+ mice. Levels of cytosolic cytochrome c and active caspase-3 were increased in SN of VPS35D620N/+ mice aged 16 months. Our results suggest that PARK17 mutant (D620N) VPS35 impairs activity of Wnt/β-catenin signaling pathway and causes abnormal morphology and dysfunction of mitochondria, which could lead to neurodegeneration of SNpc DAergic cells.
         datePublished:2020-11-30T00:00:00Z
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      headline:(D620N) VPS35 causes the impairment of Wnt/β-catenin signaling cascade and mitochondrial dysfunction in a PARK17 knockin mouse model
      description:Patients with familial type 17 of Parkinson’s disease (PARK17) manifest autosomal dominant pattern and late-onset parkinsonian syndromes. Heterozygous (D620N) mutation of vacuolar protein sorting 35 (VPS35) is genetic cause of PARK17. We prepared heterozygous VPS35D620N/+ knockin mouse, which is an ideal animal model of (D620N) VPS35-induced autosomal dominant PARK17. Late-onset loss of substantia nigra pars compacta (SNpc) dopaminergic (DAergic) neurons and motor deficits of Parkinson’s disease were found in 16-month-old VPS35D620N/+ mice. Normal function of VPS35-containing retromer is needed for activity of Wnt/β-catenin cascade, which participates in protection and survival of SNpc DAergic neurons. It was hypothesized that (D620N) VPS35 mutation causes the malfunction of VPS35 and resulting impaired activity of Wnt/β-catenin pathway. Protein levels of Wnt1 and nuclear β-catenin were reduced in SN of 16-month-old VPS35D620N/+ knockin mice. Downregulated protein expression of survivin, which is a target gene of nuclear β-catenin, and upregulated protein levels of active caspase-8 and active caspase-9 were observed in SN of VPS35D620N/+ mice at age of 16 months. VPS35 is involved in controlling morphology and function of mitochondria. Impaired function of VPS35 caused by (D620N) mutation could lead to abnormal morphology and malfunction of mitochondria. A significant decrease in mitochondrial size and resulting mitochondrial fragmentation was found in tyrosine hydroxylase-positive and neuromelanin-positive SNpc DAergic neurons of 16-month-old VPS35D620N/+ mice. Mitochondrial complex I activity or complex IV activity was reduced in SN of 16-month-old VPS35D620N/+ mice. Increased level of mitochondrial ROS and oxidative stress were found in SN of 16-month-old VPS35D620N/+ mice. Levels of cytosolic cytochrome c and active caspase-3 were increased in SN of VPS35D620N/+ mice aged 16 months. Our results suggest that PARK17 mutant (D620N) VPS35 impairs activity of Wnt/β-catenin signaling pathway and causes abnormal morphology and dysfunction of mitochondria, which could lead to neurodegeneration of SNpc DAergic cells.
      datePublished:2020-11-30T00:00:00Z
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      keywords:
         Cell death in the nervous system
         Cellular neuroscience
         Life Sciences
         general
         Biochemistry
         Cell Biology
         Immunology
         Cell Culture
         Antibodies
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