A5060641907- Neuroinflammation and Neurodegeneration Mechanisms
- Parkinson's Disease Mechanisms and Treatments
- Neuroscience and Neuropharmacology Research
- Nerve injury and regeneration
- Immune Response and Inflammation
- Signaling Pathways in Disease
- Blood Coagulation and Thrombosis Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- S100 Proteins and Annexins
- Nuclear Receptors and Signaling
- Cannabis and Cannabinoid Research
- Ion Channels and Receptors
- Alzheimer's disease research and treatments
- Olfactory and Sensory Function Studies
- Cholinesterase and Neurodegenerative Diseases
- Adenosine and Purinergic Signaling
- Autism Spectrum Disorder Research
- Sleep and Wakefulness Research
- Cellular transport and secretion
- Circadian rhythm and melatonin
- Cell death mechanisms and regulation
- Calpain Protease Function and Regulation
- Glycosylation and Glycoproteins Research
- Intracerebral and Subarachnoid Hemorrhage Research
- Biochemical effects in animals
Kyung Hee University
2014-2024
Sorbonne Paris Cité
2016
Université Paris Cité
2016
Délégation Paris 5
2016
Ajou University
2000-2009
Korea Institute of Brain Science
2009
Brain (Germany)
2005-2006
Yonsei University
2001
Seoul National University
2001
Burke Medical Research Institute
1996-1999
The present study examined whether the antidepressant paroxetine promotes survival of nigrostriatal dopaminergic (DA) neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model Parkinson's disease. MPTP induced degeneration DA and glial activation as visualized by tyrosine hydroxylase, macrophage Ag complex-1, and/or fibrillary acidic protein immunoreactivity. Real-time PCR, Western blotting, immunohistochemistry showed upregulation proinflammatory cytokines, microglial NADPH...
Currently there is no neuroprotective or neurorestorative therapy for Parkinson’s disease. Here we report that transient receptor potential vanilloid 1 (TRPV1) on astrocytes mediates endogenous production of ciliary neurotrophic factor (CNTF), which prevents the active degeneration dopamine neurons and leads to behavioural recovery through CNTF alpha (CNTFRα) nigral in both MPP+-lesioned adeno-associated virus α-synuclein rat models Western blot immunohistochemical analysis human post-mortem...
This study examined whether the cannabinoid receptor type 1 (CB(1)) contributes to survival of nigrostriatal dopaminergic (DA) neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model Parkinson's disease. MPTP induced significant loss DA and microglial activation substantia nigra (SN), visualized with tyrosine hydroxylase or macrophage Ag complex-1 immunohistochemistry. Real-time PCR, ELISA, Western blotting, immunohistochemistry disclosed upregulation proinflammatory...
Abstract The present study examined the neuroprotective effects of capsaicin (CAP) and explored their underlying mechanisms in a lipopolysaccharide (LPS)-lesioned inflammatory rat model Parkinson’s dieases (PD). LPS was unilaterally injected into substantia nigra (SN) absence or presence CAP capsazepine (CZP, TRPV1 antagonist). SN tissues were prepared for immunohistochemical staining, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, western blot blood–brain barrier (BBB)...
The cannabinoid (CB2) receptor type 2 has been proposed to prevent the degeneration of dopamine neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. However, mechanisms underlying CB2 receptor-mediated neuroprotection MPTP mice have not elucidated. substantia nigra (SN) were evaluated mouse model Parkinson's disease (PD) by immunohistochemical staining (tyrosine hydroxylase, macrophage Ag complex-1, glial fibrillary acidic protein, myeloperoxidase (MPO), and CD3...
The effects of capsaicin (CAP), a transient receptor potential vanilloid subtype 1 (TRPV1) agonist, were determined on nigrostriatal dopamine (DA) neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model Parkinson's disease (PD). results showed that TRPV1 activation by CAP rescued DA neurons, enhanced striatal functions and improved behavioral recovery MPTP-treated mice. neuroprotection was associated with reduced expression proinflammatory cytokines (tumor necrosis...
The present study examined whether thrombin-induced microglial activation could contribute to death of dopaminergic neurons in the rat substantia nigra (SN) vivo. Seven days after thrombin injection into SN, tyrosine hydroxylase immunohistochemistry showed a significant loss nigral neurons. In parallel, thrombin-activated microglia, visualized by immunohistochemical staining using antibodies against complement receptor type 3 (OX-42) and major histocompatibility complex class II antigens...
Abstract The present study examined the expression of transient receptor potential vanilloid subtype 1 (TRPV1) in microglia, and its association with microglial cell death. In vitro cultures, RT-PCR, Western blot analysis, immunocytochemical staining experiments revealed that rat microglia a human line (HMO6) showed TRPV1 expression. Furthermore, exposure these cells to agonists, capsaicin (CAP) resiniferatoxin (RTX), triggered This effect was ameliorated by antagonists, capsazepine...
The present study investigated whether thrombin, a potent microglial activator, can induce reactive oxygen species (ROS) generation through activation of NADPH oxidase and if this may contribute to oxidative damage consequent neurodegeneration. Seven days after intrahippocampal injection Nissl staining immunohistochemistry using the neuronal-specific nuclear protein NeuN revealed significant loss in hippocampal CA1 neurons. In parallel, thrombin-activated microglia, assessed by OX-42 OX-6...
Intranigral injection of the transient receptor potential vanilloid subtype 1 (TRPV1; also known as VR1) agonist capsaicin (CAP) into rat brain, or treatment mesencephalic cultures with CAP, resulted in cell death dopaminergic (DA) neurons, visualized by immunocytochemistry. This vivo and vitro effect was ameliorated TRPV1 antagonist capsazepine (CZP) iodo-resiniferatoxin, suggesting direct involvement neurotoxicity. In cultures, both CAP anandamide (AEA), an endogenous ligand for...
Epidemiological studies have reported that smoking is associated with a lower incidence of Parkinson's disease (PD), leading to theories in general and nicotine particular might be neuroprotective. Recent suggested cholinergic anti-inflammatory pathway-regulating microglial activation through alpha7 nicotinic receptors. In the present study, we used lipopolysaccharide (LPS)-induced vitro vivo inflammation models investigate whether has protective effect on dopaminergic system an mechanism....
Abstract How to minimize brain inflammation is pathophysiologically important, since induced by microglial activation can exacerbate damage. In the present report, we show that injection of lipopolysaccharide (LPS) into rat cortex led increased levels interleukin‐13 (IL‐13) and IL‐13 immunoreactivity, followed substantial loss microglia at 3 days post‐LPS. in LPS‐injected reached a peak 12 h post‐injection, remained elevated 24 h, returned basal day 4. parallel, immunoreactivity was detected...
The aim of this study was to investigate changes in protein profiles during the early phase dopaminergic neuronal death using two-dimensional gel electrophoresis conjunction with mass spectrometry. Several spots were identified whose expression significantly altered following treatment MN9D cells 6-hydroxydopamine (6-OHDA). In particular, we detected oxidative modification thioredoxin-dependent peroxidases (peroxiredoxins; PRX) treated cells. Oxidative PRX induced by 6-OHDA blocked presence...
The present study examined whether matrix metalloproteinase-3 (MMP-3) participates in the loss of dopaminergic (DA) neurons nigrostriatal pathway a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model Parkinson's disease with blood brain barrier (BBB) damage and infiltration peripheral immune cells. Tyrosine hydroxylase (TH) immunostaining sections from MPTP-treated mice showed that MPTP induced significant degeneration DA neurons. Moreover, FITC-labeled albumin detection revealed...
Two cysteine protease families, caspase and calpain, are known to participate in cell death. We investigated whether a stress‐specific activation pathway exists, what extent Bcl‐2 plays role preventing drug‐induced activity death dopaminergic neuronal line, MN9D. Staurosporine (STS) induced caspase‐dependent apoptosis while neurotoxin, MPP + largely caspase‐independent necrotic as determined by morphological biochemical criteria including cytochrome c release fluorogenic cleavage assay. At...
The present study shows that activation of microglial NADPH oxidase and production reactive oxygen species (ROS) is associated with thrombin-induced degeneration nigral dopaminergic neurons in vivo. Seven days after thrombin injection the rat substantia nigra (SN), tyrosine hydroxylase immunocytochemistry showed a significant loss neurons. This cell death was accompanied by localization terminal deoxynucleotidyl transferase-mediated fluorecein UTP nick-end labelling (TUNEL) staining within...
Because the dopaminergic pathways in midbrain have been closely associated with serious neuropsychiatric disorders, elucidation of mechanisms underlying neuronal development should provide some important clues for related disorders. In mice lacking dopamine D 2 receptor (D R−/−), stereological cell counting analysis showed that number mesencephalic tyrosine hydroxylase (TH) cells was significantly low during ontogeny, compared observed wild-type (WT) mice, thereby indicating an alteration...
A degree of brain inflammation is required for repair damaged tissue, but excessive causes neuronal cell death. Here, we observe that IL-10 expressed in LPS-injected rat cerebral cortex, contributing to survival. Cells immunopositive were detected as early 8 h post-injection and persisted up 3 d, parallel with the expression IL-1β, TNF-α, iNOS. Double immunofluorescence staining showed was localized mainly activated microglia. Next, examined neuroprotective effects using neutralizing...
In the present study, we investigated effects of IL-13, a well-known anti-inflammatory cytokine, on thrombin-treated hippocampus in vivo. NeuN immunohistochemistry and Nissl staining revealed significant loss hippocampal CA1 neurons upon intrahippocampal injection thrombin. This neurotoxicity was accompanied by substantial microglial activation, as evident from OX-42 results. parallel, Western blot analysis hydroethidine histochemistry disclosed activation NADPH oxidase, generation reactive...
This study examined whether ethyl pyruvate (EP) promotes the survival of nigrostriatal dopaminergic (DA) neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model Parkinson's disease. MPTP induced degeneration DA and glial activation as visualized by tyrosine hydroxylase, macrophage Ag complex-1, and/or fibrillary acidic protein immunoreactivity. Western blotting immunohistochemistry showed microglial NADPH oxidase astroglial myeloperoxidase (MPO) subsequent reactive oxygen...