Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8399405 | Mitochondrion | 2017 | 10 Pages |
Abstract
A water-soluble formulation of CoQ10 (WS-CoQ10) was shown to stabilize mitochondria and prevent oxidative stress-induced neuronal death. Presenilin-1 (PS-1)-mutated Alzheimer's Disease (AD) fibroblasts (PSAF) were used for studying the effects of PS-1 mutation. PS-1 mutation correlated to increased reactive oxygen species (ROS) production and stress induced premature senescence (SIPS) in PSAF; WS-CoQ10 treatment decreased ROS generation, increased population doublings, and postponed SIPS. Treated PSAF had higher PCNA expression, and lower levels of MnSOD, p21, p16Ink4A, and Rb. WS-CoQ10 caused the resumption of autophagy in PSAF. Thus, WS-CoQ10 as inhibitor of SIPS and ameliorator of autophagy could be an effective prophylactic/therapeutic agent for AD.
Keywords
PS-1Presenilin-1SA-β-galTBSTLC3CoQ10MnSODPTSTMRMMDCAPPHBSSV-ATPaseNHFRFUMMPPBSPCNADICPS-2DcfAβ2′,7′-dichlorofluoresceinH2DCFDApresenilin-2ROSProliferating Cell Nuclear AntigenAutophagysodium dodecyl sulfate-polyacrylamide gel electrophoresisSDS-PAGEsenescence-associated beta-galactosidaseAlzheimer's diseaseTris-buffered saline Tween-20retinoblastomamanganese superoxide dismutaseSipsPhosphate buffered salinetetramethylrhodamine methyl esterHank's balanced salt solutionMonodansylcadaverineMitochondriaRelative Fluorescence UnitsMitochondrial membrane potentialmicrotubule-associated protein 1 light chain 3amyloid precursor proteinamyloid-beta peptideSenescenceStress-induced premature senescencedifferential interference contrastCoenzyme Q10Reactive oxygen species
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Authors
Dennis Ma, Kyle Stokes, Kevinjeet Mahngar, Danijela Domazet-Damjanov, Marianna Sikorska, Siyaram Pandey,