| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 11016204 | Nanomedicine: Nanotechnology, Biology and Medicine | 2019 | 36 Pages |
Abstract
SPIO-NPs, but not GO-QDs, trigger ROS overproduction and mitochondrial disrupt in hepatic cells, leading to the increase in PINK1 stability. PINK1 then recruits and phosphorylates PARKIN at Ser65. The p-PARKIN ubiquitinates the proteins at mitochondrial outer membrane (MOM). Once MOM proteins are ubiquitinated by PARKIN, the ubiquitins are recruited to the damaged mitochondria that fuse to lysosomes with the help of LC3-II and go through PINK1-dependent mitophagy. Mitophagy-based HCA has been proven to be an efficient, early, and sensitive screening method to incorporate into current HCA nanosafety assessment system.225
Keywords
HCAPLADLSCdTeMMPDAPIPBSSPIONMSQDsPINK14’,6-diamidino-2-phenylindoleNPsPTEN-induced putative kinase 1Small interfering RNAROSsiRNA[Ca2+]iProximity ligation assayMRISuperparamagnetic iron oxideZnOZinc oxideCeO2Graphene oxideTemHigh-content analysisMagnetic resonance imagingCadmium tellurideIntracellular Ca2+cerium dioxideSiO2Silicon dioxideGoldmitochondrial outer membraneMoMphosphate buffered solutionMitophagyTransmission electron microscopyNanomaterialsNanoparticlesSuperparamagnetic iron oxide nanoparticlesquantum dotsMitochondrial membrane potentialDynamic Light Scattering
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Authors
Chengyong PhD, Shengwei MS, Huan BS, Liyin BS, Chuanli BS, Shan BS, Fengkai BS, Denglin BS, Gang PhD, Zhongning PhD, Yuchun PhD, Xiaoyuan PhD,