A5085311837- Axon Guidance and Neuronal Signaling
- Neuroscience and Neuropharmacology Research
- Neurogenesis and neuroplasticity mechanisms
- Neuroinflammation and Neurodegeneration Mechanisms
- RNA Interference and Gene Delivery
- Cancer-related Molecular Pathways
- Nerve injury and regeneration
- Angiogenesis and VEGF in Cancer
- Cell death mechanisms and regulation
- Multiple Sclerosis Research Studies
- Circadian rhythm and melatonin
- Barrier Structure and Function Studies
- Photoreceptor and optogenetics research
- Adenosine and Purinergic Signaling
- Mitochondrial Function and Pathology
- Zebrafish Biomedical Research Applications
- Cancer, Hypoxia, and Metabolism
- Genetics, Aging, and Longevity in Model Organisms
- Selenium in Biological Systems
- Neuroscience and Neural Engineering
- DNA Repair Mechanisms
- Stress Responses and Cortisol
- Sperm and Testicular Function
- Nuclear Receptors and Signaling
- Medicinal Plants and Neuroprotection
Southern University of Science and Technology
2016-2025
Beijing Chao-Yang Hospital
2025
Capital Medical University
2025
Huashan Hospital
2023
National Clinical Research
2023
University of Ottawa
2006-2020
Wenzhou Medical University
2009-2019
First Affiliated Hospital of Wenzhou Medical University
2014-2019
National Natural Science Foundation of China
2017
National Research Council Canada
2005-2016
Although the neurogenesis-enhancing effects of exercise have been extensively studied, molecular mechanisms underlying this response remain unclear. Here, we propose that is mediated by exercise-induced systemic release antioxidant selenium transport protein, selenoprotein P (SEPP1). Using knockout mouse models, confirmed SEPP1 and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) are required for increase in adult hippocampal neurogenesis. In vivo infusion increased...
Although B-amyloid (AB) is suggested to play an important role in Alzheimer's disease, the mechanisms that control AB-evoked toxicity are unclear. We demonstrated previously cell cycle-related cyclin-dependent kinase 4/6/retinoblastoma protein pathway required for AB-mediated death. However, downstream target(s) of this unknown. show here neurons lacking E2F1, a transcription factor regulated by retinoblastoma protein, significantly protected from death evoked AB. Moreover, p53 deficiency...
Abstract The complex relationship between specific hippocampal oscillation frequency deficit and cognitive dysfunction in the ischemic brain is unclear. Here, using a mouse two-vessel occlusion (2VO) cerebral ischemia model, we show that visual stimulation with 40 Hz light flicker drove CA1 slow gamma restored 2VO-induced reduction power theta-low phase-amplitude coupling, but not those of high gamma. Low lights at 30 Hz, 50 10 80 arrhythmic light, were protective against degenerating...
Optogenetics is a valuable tool for studying the mechanisms of neurological diseases and now being developed therapeutic applications. In rodents macaques, improved channelrhodopsins have been applied to achieve transcranial optogenetic stimulation. While photoexcitation neurons has achieved, noninvasive inhibition treating hyperexcitability-induced disorders remained elusive. There critical need effective inhibitory tools that are highly light-sensitive capable suppressing neuronal activity...
Growing evidence suggests that certain cell cycle regulators also mediate neuronal death. Of relevance, cyclin D1-associated kinase activity is increased and the retinoblastoma protein (Rb), a substrate of D1-Cdk4/6 complex, phosphorylated during K<sup>+</sup> deprivation-evoked death cerebellar granule neurons (CGNs). Cyclin-dependent (CDK) inhibitors block this death, suggesting requirement for D1/Cdk4/6-Rb pathway. However, downstream target(s) pathway are not well defined. The...
Gangliosides, a member of the glycosphingolipid family, are heterogeneously expressed in biological membranes and particularly enriched within central nervous system. Gangliosides consist mono- or poly-sialylated oligosaccharide chains variable lengths attached to ceramide unit found be intimately involved brain disease development. The purpose this study is examine spatial profile ganglioside species using matrix-assisted laser desorption/ionization (MALDI) imaging (IMS) following middle...
Semaphorin 3A (Sema3A) increased significantly in mouse brain following cerebral ischemia. However, the role of Sema3A stroke remains unknown. Our aim was to determine wether functions as a vascular permeability factor and contributes ischemic damage. Recombinant injected intradermally skin, or stereotactically into cortex, caused dose- time-dependent increases permeability, with degree comparable that by injection known endothelial growth receptors (VEGF). Application cultured cells...
Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by social communication deficiencies and stereotypic behaviors influenced hereditary and/or environmental risk factors. There are currently no approved medications for treating the core symptoms of ASD. Human fecal microbiota transplantation (FMT) has emerged as potential intervention to improve autistic symptoms, but underlying mechanisms not fully understood. In this study, we evaluated effects...
Abstract : The transcription factor E2F1 is known to mediate apoptosis in isolated quiescent and postmitotic cardiac myocytes, its absence decreases the size of brain infarction following cerebral ischemia. To demonstrate directly that modulates neuronal apoptosis, we used cultured cortical neurons show a temporal association expression with increased apoptosis. Cortical lacking (derived from ‐/‐ mice) were resistant staurosporine‐induced as evidenced by significantly lower caspase 3‐like...
Collapsin response mediator proteins (CRMPs) mediate growth cone collapse during development, but their roles in adult brains are not clear. Here we report the findings that full-length CRMP-3 (p63) is a direct target of calpain cleaves at N terminus (+76 amino acid). Interestingly, activated to excitotoxicity vitro and cerebral ischemia vivo also cleaved CRMP-3, cleavage product (p54) underwent nuclear translocation neuronal death. The expression p54 was colocalized with terminal...
Inhibitors of HIV protease have been shown to antiapoptotic effects in vitro, yet whether these are seen vivo remains controversial. In this study, we evaluated the impact inhibitor (PI) nelfinavir, boosted with ritonavir, models nonviral disease associated excessive apoptosis. mice Fas-induced fatal hepatitis, Staphylococcal enterotoxin B-induced shock, and middle cerebral artery occlusion-induced stroke, demonstrate that PIs significantly reduce apoptosis improve histology, function,...
Abstract Intracellular calcium influx through NMDA receptors triggers a cascade of deleterious signaling events which lead to neuronal death in neurological conditions such as stroke. However, it is not clear the molecular mechanism underlying early damage response from axons and dendrites are important maintaining network essential for survival neurons. Here, we examined changes treated with glutamate showed appearance βIII‐tubulin positive varicosities on before death. Dizocilpine blocked...
Despite progress in reperfusion therapy, functional recovery remains suboptimal many stroke patients, with oxidative stress, inflammation, dysbiosis, and secondary neurodegeneration constituting the major hurdles to recovery. The essential trace element selenium is emerging as a promising therapeutic agent for stroke. However, although several rodent studies have shown that can protect against cell loss following cerebral ischemia, no study has yet examined whether enhance long-term...
Abstract Perineuronal nets (PNNs) which mostly surround the parvalbumin (PV) neurons, have been shown to play critical roles in neural plasticity. Recently, PNNs regulate fear‐associated memory, but molecular mechanism is still unclear. In this study, we found that removal of vivo using chondroitinase ABC (ChABC) injection resulted reduced firing rate PV neurons and decreased inhibitory synaptic transmission both excitatory CA1 hippocampus. Interestingly, altered appears be mediated by...
Microglia are the 'immune cells' of brain and their activation plays a vital role in pathogenesis many neurodegenerative diseases. Activated microglia produce high levels pro-inflammatory factors, such as TNFα, causing neurotoxicity. Here we show that vimentin played key controlling neurotoxicity during cerebral ischemia. Deletion expression significantly impaired response to LPS vitro transient focal ischemia vivo. Reintroduction functional gene back into knockout restored LPS. More...
To investigate whether curcumin regulates Notch signaling to cause neuroprotection and neurogenesis after focal ischemia reperfusion injury.Focal injury was modeled in rats by occluding the middle cerebral artery. These animals were given either (300 mg/kg) or corn oil (vehicle) intraperitoneal injection starting 1 h stroke continuing for 7 d. In parallel, sham-operated control received vehicle. All killed on day 12. The different treatment groups compared terms of neurobehavioral deficits,...
Various pathological characteristics of autism spectrum disorder (ASD) stem from abnormalities in brain resident immune cells, specifically microglia, to prune unnecessary synapses or neural connections during early development. Animal models ASD exhibit an abundance different regions, which is strongly linked the appearance behaviors. Overexpression CD47 on neurons acts as a “don’t eat me” signal, safeguarding inappropriate pruning by microglia. Indeed, overexpression occurs 16p11.2...
Minocycline is a potent neuroprotective tetracycline in animal models of cerebral ischemia. We examined the protective properties chlortetracycline (CTC) and demeclocycline (DMC) showed that these two tetracyclines were also against glutamate-induced neuronal death vitro ischemia vivo. However, CTC DMC appeared to confer neuroprotection through unique mechanism compared with minocycline. Rather than inhibiting microglial activation caspase, suppressed calpain activities. In addition, only...
Aberrant activation of the Rb/E2F1 pathway in cycling cells, response to mitogenic or nonmitogenic stress signals, leads apoptosis through hyperphosphorylation Rb. To test whether postmitotic neurons can be activated by signaling, we examined role p38 stress-activated protein kinase (SAPK) regulating Rb phosphorylation Fas (CD95/APO1)-mediated cultured cerebellar granule (CGNs). Anti-Fas antibody induced a dramatic and early p38. Activated was correlated with induction both endogenous...