A5100397905- Axon Guidance and Neuronal Signaling
- Traumatic Brain Injury and Neurovascular Disturbances
- Neurobiology and Insect Physiology Research
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Phagocytosis and Immune Regulation
- interferon and immune responses
- Hereditary Neurological Disorders
- Cerebrospinal fluid and hydrocephalus
- S100 Proteins and Annexins
- Barrier Structure and Function Studies
- Erythrocyte Function and Pathophysiology
- Genetic Neurodegenerative Diseases
- Photoreceptor and optogenetics research
- Tryptophan and brain disorders
- Insect and Arachnid Ecology and Behavior
- Inflammasome and immune disorders
- Nerve injury and regeneration
- Treatment of Major Depression
- Physiological and biochemical adaptations
- Neurogenesis and neuroplasticity mechanisms
- Immune Response and Inflammation
- Immune cells in cancer
- Insect and Pesticide Research
- Angiogenesis and VEGF in Cancer
Sericultural Research Institute
2020-2025
Foshan University
2023
Virginia Tech
2019-2023
Virginia–Maryland College of Veterinary Medicine
2019-2023
Zhejiang University
2022
West China Medical Center of Sichuan University
2022
National Institute of Biological Sciences, Beijing
2022
Smith-Kettlewell Eye Research Institute
2021
Massachusetts Eye and Ear Infirmary
2021
Chinese Academy of Medical Sciences & Peking Union Medical College
2017-2020
Abstract Life experience can leave lasting marks, such as epigenetic changes, in the brain. How life is translated into storable information remains largely unknown. With unbiased data-driven approaches, we predicted that Egr1 , a transcription factor important for memory formation, plays an essential role brain programming. We performed EGR1 ChIP-seq and validated thousands of binding sites with methylation patterns established during postnatal development. More specifically, these become...
The scavenger receptor CD36 is injurious in acute experimental focal stroke and neurodegenerative diseases the adult. We investigated effects of genetic deletion (CD36ko) on injury, oxidative inflammatory signaling after neonatal stroke.
Inflammation is a significant contributor to neuronal death and dysfunction following traumatic brain injury (TBI). Recent evidence suggests that interferons may be key regulator of this response. Our studies evaluated the role Cyclic GMP-AMP Synthase-Stimulator Interferon Genes (cGAS-STING) signaling pathway in murine model TBI. Male, 8-week old wildtype, STING knockout (-/-), cGAS -/-, NLRX1 -/- mice were subjected controlled cortical impact (CCI) or sham injury. Histopathological...
Although age-at-injury influences chronic recovery from traumatic brain injury (TBI), the differential effects of age on early outcome remain understudied. Using a male murine model moderate contusion injury, we investigated underlying mechanism(s) regulating distinct response between juvenile and adult TBI. We demonstrate similar biomechanical physical properties naive brains. However, following controlled cortical impact (CCI), mice displayed reduced lesion formation, cell death,...
To adapt to environmental changes, diapausing silkworm eggs remain dormant during the early stages of embryonic development. Various methods have been used terminate egg diapause and promote hatching. elucidate molecular mechanisms by which corona other treatments diapause, we collected at 1, 6, 20 h after sequenced their transcriptomes. The results showed that both hydrochloric acid (HCl) effectively terminated promoted hatching, with treatment inducing faster hatching than HCl treatment....
Leptomeningeal anastomoses or pial collateral vessels play a critical role in cerebral blood flow (CBF) restoration following ischemic stroke. The magnitude of this adaptive response is postulated to be controlled by the endothelium, although underlying molecular mechanisms remain under investigation. Here we demonstrated that endothelial genetic deletion, using EphA4fl/fl/Tie2-Cre and EphA4fl/fl/VeCahderin-CreERT2 mice vessel painting strategies, implicated EphA4 receptor tyrosine kinase as...
Neurobiological consequences of traumatic brain injury (TBI) result from a complex interplay secondary responses and sequela that mediates chronic disability. Endothelial cells are important regulators the cerebrovascular response to TBI. Our work demonstrates genetic deletion endothelial cell (EC)-specific EPH receptor A4 (EphA4) using conditional EphA4 f/f /Tie2-Cre /VE-Cadherin-CreERT2 knockout (KO) mice promotes blood–brain barrier (BBB) integrity tissue protection, which correlates with...
Abstract Background The continuum of pro- and anti-inflammatory response elicited by traumatic brain injury (TBI) is suggested to play a key role in the outcome TBI; however, underlying mechanisms remain ill -defined. Methods Here, we demonstrate that using bone marrow chimeric mice systemic inhibition EphA4 receptor shifts pro-inflammatory milieu pro-resolving following acute TBI. Results expression increased injured cortex as early 2 h post-TBI on CX3CR1 gfp -positive cells peri-lesion....
Abstract Background Efferocytosis is a process that removes apoptotic cells and cellular debris. Clearance of these alleviates neuroinflammation, prevents the release inflammatory molecules, promotes production anti-inflammatory cytokines to help maintain tissue homeostasis. The underlying mechanisms by which this occurs in brain after injury remain ill-defined. Methods We used GFP bone marrow chimeric knockout (KO) mice demonstrate axon guidance molecule EphA4 receptor tyrosine kinase...
Cell replacement therapy using neural stem cells (NSCs) transplantation has recently emerged as a promising method of Parkinson's disease (PD) treatment; however, the underlying mechanisms are not fully understood. To gain new insights into 6-hydroxydopamine (6-OHDA)-induced lesioning and therapeutic efficacy human NSCs (hNSCs) transplantation, striatum (ST) intrastriatal 6-OHDA-injected parkinsonian mice were unilaterally engrafted with undifferentiated hNSCs. A high-throughput quantitative...
Circulating monocytes have emerged as key regulators of the neuroinflammatory milieu in a number neuropathological disorders. Ephrin type A receptor 4 (Epha4) tyrosine kinase, prominent axon guidance molecule, has recently been implicated regulation neuroinflammation. Using mouse model brain injury and GFP BM chimeric approach, we found neuroprotection lack significant motor deficits marked by reduced monocyte/macrophage cortical infiltration an increased arginase-1+ cells absence BM-derived...
Epileptic networks are characterized as having two states, seizures or more prolonged interictal periods. However, cellular mechanisms underlying the contribution of periods to ictal events remain unclear. Here, we use an activity-dependent labeling technique combined with genetically encoded effectors characterize and manipulate neuronal ensembles recruited by focal (FS-Ens) (IP-Ens) in piriform cortex, a region that plays key role seizure generation. Ca2+ activities histological evidence...
Erythropoietin-producing human hepatocellular receptors play a major role in central nervous system injury. Preclinical and clinical studies revealed the upregulation of erythropoietin-producing A4 (EphA4) brain after acute traumatic We have previously reported that Cx3cr1-expressing cells peri-lesion show high levels EphA4 induction controlled cortical impact (CCI) injury mice. Cx3cr1 is fractalkine receptor expressed on both resident microglia peripheral-derived macrophages. The current...
Abstract Brain injury resulting from repeated mild traumatic insult is associated with cognitive dysfunction and other chronic co-morbidities. The current study tested the effects of aberrant neurogenesis in a mouse model brain (rmTBI). Using Barnes Maze analysis, we found significant reduction spatial learning memory at 24 days post-rmTBI compared to sham (rSham) injury. Cell fate analysis showed greater number BrdU-labeled cells which co-expressed Prox-1 DG rmTBI-injured mice coincided...
Epilepsy is a circuit-level brain disorder characterized by hyperexcitatory seizures with unclear mechanisms. Here, we investigated the causal roles of calretinin (CR) neurons in posterior intralaminar thalamic nucleus (PIL) hippocampal seizures. Using c-fos mapping and calcium fiber photometry, found that PIL CR were activated during kindling model. Optogenetic activation accelerated seizure development, whereas inhibition retarded development. Further, viral-based circuit tracing verified...
Abstract Familial dysautonomia (FD) is an autosomal recessive neurodegenerative disease caused by a splicing mutation in the gene encoding Elongator complex protein 1 (ELP1, also known as IKBKAP). This results tissue-specific skipping of exon 20 with corresponding reduction ELP1 protein, predominantly central and peripheral nervous system. Although FD patients have neurological phenotype continuous depletion sensory autonomic neurons, progressive visual decline leading to blindness one most...
Efferocytosis is a process that removes apoptotic cells and cellular debris. Clearance of these alleviates neuroinflammation prevents the release inflammatory molecules promotes production anti-inflammatory cytokines to help maintain tissue homeostasis. The underlying mechanisms by which this occurs in brain after injury remains ill-defined.