A5026821055- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Neuroscience and Neuropharmacology Research
- Dietary Effects on Health
- Mitochondrial Function and Pathology
- Adipose Tissue and Metabolism
- Cell death mechanisms and regulation
- Extracellular vesicles in disease
- RNA Interference and Gene Delivery
- Cancer-related molecular mechanisms research
- Neurological Disease Mechanisms and Treatments
- Computational Drug Discovery Methods
- Diet and metabolism studies
- Cancer, Hypoxia, and Metabolism
- MicroRNA in disease regulation
- Biochemical effects in animals
- RNA regulation and disease
- Autophagy in Disease and Therapy
- Signaling Pathways in Disease
- Inflammasome and immune disorders
- NF-κB Signaling Pathways
- Tryptophan and brain disorders
- Neurogenesis and neuroplasticity mechanisms
- Glycosylation and Glycoproteins Research
Sungkyunkwan University
2016-2025
Samsung (South Korea)
2015-2025
Advanced Institute of Convergence Technology
2024-2025
Seoul National University
2021-2024
Seoul National University Hospital
2011-2021
Dankook University
2021
CHA University
2021
Real Academia Española
2019
Real Sociedad Española de Química
2019
National Institute on Aging
2005-2014
The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited cells. We now report that neurons express several TLRs, levels TLR2 -4 are increased in response IFN-γ stimulation energy deprivation. Neurons from both knockout mutant mice were protected against deprivation-induced cell death, which was associated with decreased activation proapoptotic signaling cascade involving jun N-terminal...
Multi-protein complexes called inflammasomes have recently been identified and shown to contribute cell death in tissue injury. Intravenous immunoglobulin (IVIg) is an FDA-approved therapeutic modality used for various inflammatory diseases. The objective of this study investigate dynamic responses the NLRP1 NLRP3 stroke determine whether can be targeted with IVIg intervention. Primary cortical neurons were subjected glucose deprivation (GD), oxygen–glucose (OGD) or simulated...
Abstract Sequential cleavages of the β‐amyloid precursor protein cleaving enzyme 1 (BACE1) by β‐secretase and γ‐secretase generate amyloid β‐peptides, believed to be responsible synaptic dysfunction neuronal cell death in Alzheimer’s disease (AD). Levels BACE1 are increased vulnerable regions AD brain, but underlying mechanism is unknown. Here we show that oxidative stress (OS) stimulates expression a requiring activity involving c‐ jun N‐terminal kinase (JNK)/c‐ pathway. levels response OS...
Excessive mitochondrial fission is a prominent early event and contributes to dysfunction, synaptic failure, neuronal cell death in the progression of Alzheimer's disease (AD). However, it remains be determined whether inhibition excessive beneficial mammal models AD. To determine dynamin-related protein 1 (Drp1), key regulator fragmentation, can disease-modifying therapeutic target for AD, we examined effects Drp1 inhibitor on dysfunctions induced by oligomeric amyloid-β (Aβ) neurons...
Osteoarthritis (OA) is a chronic degenerative disease of articular cartilage that the most common joint worldwide. Mesenchymal stem cells (MSCs) have been extensively explored for treatment OA. Recently, it has demonstrated MSC-derived extracellular vesicles (EVs) may contribute to potential mechanisms MSC-based therapies. In this study, we investigated therapeutic human adipose-derived EVs (hASC-EVs) in alleviating OA, along with mechanism. were isolated from culture supernatants hASCs by...
Significance Considering that Alzheimer’s disease (AD) is a chronic progressing over long period of time, even slight increase BACE1 expression may have profound effect on Aβ accumulation. We describe previously unknown mechanism negatively regulates and BACE1-AS demonstrate its pivotal role in the progression Tau pathologies cognitive impairment two mouse models AD. Given recent failures clinical trials using enzymatic inhibitors BACE1, it critical to explore alternative approaches such as...
Surface engineering of exosomes enhances the therapeutic efficacy rheumatoid arthritis by macrophage reprogramming.
Osteoporosis is one of the most common skeletal disorders caused by imbalance between bone formation and resorption, resulting in quantitative loss tissue. Since stem cell-derived extracellular vesicles (EVs) are growing attention as novel cell-free therapeutics that have advantages over parental cells, therapeutic effects EVs from adipose tissue-derived cells (ASC-EVs) on osteoporosis pathogenesis were investigated. ASC-EVs isolated a multi-filtration system based tangential flow filtration...
Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed brain tissue from AD patients. Base excision repair (BER) primary pathway for small base modifications such as alkylation, deamination oxidation. In this study, we have investigated alterations BER capacity brains We employed set functional assays measure activities short post-mortem interval autopsies 10 sporadic patients age-matched controls. were...
The plasma membrane (PM) contains redox enzymes that provide electrons for energy metabolism and recycling of antioxidants such as coenzyme Q alpha-tocopherol. Brain aging neurodegenerative disorders involve impaired oxidative damage, but the involvement PM system (PMRS) in these processes is unknown. Caloric restriction (CR), a manipulation protects brain against disease, increased activities PMRS (NADH-ascorbate free radical reductase, NADH-quinone oxidoreductase 1, NADH-ferrocyanide...
Stroke is among the three leading causes of death worldwide and most frequent cause permanent disability. Brain ischemia induces an inflammatory response involving activated complement fragments. Here we show that i.v. Ig (IVIG) treatment, which scavenges fragments, protects brain cells against deleterious effects experimental reperfusion (I/R) prevents I/R-induced mortality in mice. Animals administered IVIG either 30 min before or after 3 h exhibited a 50–60% reduction infarct size 2- to...
The Notch signaling pathway is critically involved in cell fate decisions during development of many tissues and organs. In the present study we employed vivo culture models to elucidate role wound healing. healing full-thickness dermal wounds was significantly delayed antisense transgenic mice normal treated with γ-secretase inhibitors that block proteolytic cleavage activation Notch. contrast, a ligand Jagged peptide showed enhanced compared controls. Activation or inhibition altered...
Among various proinflammatory cytokines involved in the pathogenesis of rheumatoid arthritis (RA), tumor necrosis factor (TNF)-α plays a pivotal role release other and induction chronic inflammation. Even though siRNA has therapeutic potential, they have challenge to be delivered into target cells because their poor stability physiological fluids. Herein, we design nanocomplex polymerized (poly-siRNA) targeting TNF-α with thiolated glycol chitosan (tGC) polymers for treatment RA. Poly-siRNA...
Background and Purpose— Activation of Notch worsens ischemic brain damage as antisense knockdown or pharmacological inhibition the pathway reduces infarct size improves functional outcome in a mouse model stroke. We sought to determine whether activation contributes postischemic inflammation by directly modulating microglial innate response. Methods— The response attendant inflammatory reaction were evaluated Notch1 transgenic (Tg) nontransgenic (non-Tg) mice subjected middle cerebral artery...