Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microglial activation is known to be an important event during innate immunity, but microglial inflammation is also thought to play a role in the etiology of neurodegenerative diseases. Recently, it was reported that autophagy could influence inflammation and activation of microglia. However, little is known about the regulation of autophagy during microglial activation. In this study, we demonstrated that mitochondrial fission-induced ROS can promote autophagy in microglia. Following LPS-induced autophagy, GFP-LC3 puncta were increased, and this was suppressed by inhibiting mitochondrial fission and mitochondrial ROS. Interestingly, inhibition of mitochondrial fission and mitochondrial ROS also resulted in decreased p62 expression, but Beclin1 and LC3B were unaffected. Taken together, these results indicate that ROS induction due to increased LPS-stimulated mitochondrial fission triggers p62 mediated autophagy in microglial cells. Our findings provide the first important clues towards understanding the correlation between mitochondrial ROS and autophagy. Abbreviations: Drp1; Dynamin related protein 1, LPS; Lipopolysaccharide, ROS; Reactive Oxygen Species, GFP; Green Fluorescent Protein, CNS; Central Nervous System, AD; Alzheimer's Disease, PD; Parkinson's Disease, ALIS; Aggresome-like induced structures, iNOS; inducible nitric oxide synthase, Cox-2; Cyclooxygenase-2, MAPK; Mitogen-activated protein kinase; SODs; Superoxide dismutase, GPXs; Glutathione Peroxidase, Prxs; Peroxiredoxins.
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PMID:Drp1-dependent mitochondrial fission regulates p62-mediated autophagy in LPS-induced activated microglial cells. 3047 54

Oxidative stress linked to the etiology of Parkinson's disease, which is characterized by chronic and progressive neurodegeneration of dopamine neurons. Superoxide dismutase enzymes (SODs) regarded as the first line of defense against oxidative damage. This study assessed the potential associations of gene polymorphisms in SOD1 (encoding Cu/Zn-SOD), SOD2 (encoding Mn-SOD) and SOD3 (encoding extracellular-SOD) with susceptibility to Parkinson's disease. A case-control study, including Parkinson's disease cases (n = 356) and controls (n = 370). Single nucleotide polymorphisms of SOD1 (rs2070424 A/G), SOD2 (rs4880 T/C) and SOD3 (rs1799895, C/G) were genotyped. Results indicated that AG or GG genotype carriers in SOD1 had a much greater risk of Parkinson's disease compared to corresponding AA genotypes, and allele G carriers had increased risk versus allele A carriers in the single nucleotide polymorphism (rs2070424 A/G) in SOD1. Further, TC or CC genotype carriers in SOD2 had a much higher risk of Parkinson's disease compared with corresponding TT genotypes, and the C carriers had an increased risk over allele T carriers in the single nucleotide polymorphism (rs4880 T/C) in SOD2. Together, carrying allele G in the single nucleotide polymorphism (rs2070424 A/G) in SOD1, or allele C in the single nucleotide polymorphism (rs4880 T/C) in SOD2, enhances genetic susceptibility to Parkinson's disease.
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PMID:Superoxide dismutase coding of gene polymorphisms associated with susceptibility to Parkinson's disease. 3160 Oct 79


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