한빛사 논문
Hyojin Leea,1,*, Seongchan Kima,1, Kyeong Seob Hwangb,c,1, Nu Ri Limd,e,1, Han Bin Ohe, Il-Joo Chob,f,g,h, Jongbaeg Kimb,*, Ki Hun Kimd,*, Hong Nam Kimb,f,h,c,*
aCenter for Biomaterials, Biomedical Engineering Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Republic of Korea
bBrain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Republic of Korea
cSchool of Mechanical Engineering, Yonsei University, Seoul, 03722, Republic of Korea
dDoping Control Center, Korea Institute of Science and Technology (KIST), Seoul, 02792, Republic of Korea
eDepartment of Chemistry, Sogang University, Seoul, 04107, South Korea
fDivision of Bio-Medical Science and Technology, KIST School, Korea University of Science and Technology, Seoul, 02792, Republic of Korea
gSchool of Electrical and Electronics Engineering, Yonsei University, Seoul, 03722, Republic of Korea
hYonsei-KIST Convergence Research Institute, Yonsei University, Seoul, 03722, Republic of Korea
1These authors contributed equally to this study.
*Corresponding authors
Abstract
Despite growing concerns regarding the threat of airborne nanoparticle-mediated brain degeneration, the underlying pathological mechanisms remain unclear. Carbon nanomaterials, the main components of airborne nanoparticles, have multi-dimensional structures. Therefore, the dimensional effect of carbon-based nanomaterials on the regulation of neural function in brain disorders requires additional clarification. Herein, we report the interaction between zero-to three-dimensional carbon nanostructures and the amyloid-beta protein, which can either activate or interrupt neuronal functions, depending on the dimension of the carbon nanostructures. The carbon nanomaterials induced significant cellular activation by short-term exposure, while prolonged exposure eventually caused neuronal cell death. Such dimension-dependent activation or degeneration was more evident in the higher-dimension carbon nanomaterials, as confirmed by the increases in neurotransmitter secretion and synapse-related protein levels to more than five times at 72 h of monitoring and calcium signaling in the neurons. The inclusion of amyloid-beta proteins ameliorated the cytotoxic effects of carbon nanomaterials in higher-dimensional carbon nanomaterials by regulating 333 genes. We found that the ɑ-synuclein gene is the key factor in carbon-induced abnormal neuronal function. Therefore, through biological analyses and in vitro feasibility studies, this new insight may contribute toward understanding the pathological mechanism and finding a new target for therapy in human brain pathologies.
Keywords : Carbon nanomaterial, Dimension, Neuron, Neurotransmitter, ɑ-synuclein
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