A5088841044- Spinal Cord Injury Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Nerve injury and regeneration
- Traumatic Brain Injury and Neurovascular Disturbances
- Autophagy in Disease and Therapy
- Extracellular vesicles in disease
- Neuroscience and Neuropharmacology Research
- Neonatal and fetal brain pathology
- Pain Mechanisms and Treatments
- Circular RNAs in diseases
- Signaling Pathways in Disease
- MicroRNA in disease regulation
- Spinal Dysraphism and Malformations
- Mesenchymal stem cell research
- S100 Proteins and Annexins
- Anesthesia and Neurotoxicity Research
- Toxoplasma gondii Research Studies
- Heme Oxygenase-1 and Carbon Monoxide
- Memory and Neural Mechanisms
- Immune Response and Inflammation
- Metabolomics and Mass Spectrometry Studies
- Intensive Care Unit Cognitive Disorders
- Cell death mechanisms and regulation
- Axon Guidance and Neuronal Signaling
University of Maryland, Baltimore
2016-2025
The University of Adelaide
2023-2024
Shaanxi Provincial People's Hospital
2023
Shanxi Medical University
2022
Shaanxi Provincial People's Hospital
2022
Xiangya Hospital Central South University
2021
Central South University
2021
Rutgers, The State University of New Jersey
2007-2020
Umeå University
2015-2019
Wuhan Institute of Physics and Mathematics
2010-2017
Chronic neuroinflammation with sustained microglial activation occurs following severe traumatic brain injury (TBI) and is believed to contribute subsequent neurodegeneration neurological deficits. Microglia, the primary innate immune cells in brain, are dependent on colony stimulating factor 1 receptor (CSF1R) signaling for their survival. In this preclinical study, we examined effects of delayed depletion chronically activated microglia functional recovery up 3 months postinjury. A CSF1R...
Experimental spinal cord injury (SCI) causes chronic neuropathic pain associated with inflammatory changes in thalamic regulatory sites. Our recent studies examining mechanisms after rodent SCI showed not only thalamus, but also other regions including hippocampus and cerebral cortex. Because appeared similar to those our TBI models that are neurodegeneration neurobehavioral dysfunction, we examined effects of mouse on cognition, depressive-like behavior, brain inflammation. caused spatial...
Abstract Autophagy is a catabolic mechanism facilitating degradation of cytoplasmic proteins and organelles in lysosome-dependent manner. flux necessary for normal neuronal homeostasis its dysfunction contributes to cell death several neurodegenerative diseases. Elevated autophagy has been reported after spinal cord injury (SCI); however, mechanism, type specificity relationship are unknown. Using rat model contusive SCI, we observed accumulation LC3-II-positive autophagosomes starting at...
Neuropsychological deficits, including impairments in learning and memory, occur after spinal cord injury (SCI). In experimental SCI models, we others have reported that such changes reflect sustained microglia activation the brain is associated with progressive neurodegeneration. present study, examined effect of pharmacological depletion on posttraumatic cognition, depressive-like behavior, pathology mice. Methods: Young adult male C57BL/6 mice were subjected to moderate/severe thoracic...
Excessive and prolonged neuroinflammation following traumatic brain injury (TBI) contributes to long-term tissue damage poor functional outcomes. However, the mechanisms contributing exacerbated inflammatory responses after remain poorly understood. Our previous work showed that macroautophagy/autophagy flux is inhibited in neurons TBI mice neuronal cell death. In present study, we demonstrate autophagy also activated microglia infiltrating macrophages, this potentiates injury-induced...
Lipofuscin is an autofluorescent (AF) pigment formed by lipids and misfolded proteins, which accumulates in postmitotic cells with advanced age. Here, we immunophenotyped microglia the brain of old C57BL/6 mice (>18 months old) demonstrate that comparison to young mice, one-third are AF, characterized profound changes lipid iron content, phagocytic activity, oxidative stress. Pharmacological depletion eliminated AF following repopulation reversed microglial dysfunction. Age-related...
MicroRNAs (miRs) are small noncoding RNAs that negatively regulate gene expression at the post-transcriptional level. To identify miRs may neuronal cell death after experimental traumatic brain injury (TBI), we profiled miR changes during first several days controlled cortical impact (CCI) in mice. miR-23a and miR-27a were rapidly downregulated injured cortex hour TBI. These coincided with increased of proapoptotic Bcl-2 family members Noxa, Puma, Bax. In an etoposide-induced <i>in vitro</i>...
Abstract Necroptosis, a regulated necrosis pathway mediated by the receptor-interacting protein kinases 1 and 3 (RIPK1 RIPK3), is induced following spinal cord injury (SCI) thought to contribute neuronal glial cell death. However, mechanisms leading activation of necroptosis after SCI remain unclear. We have previously shown that autophagy, catabolic facilitating degradation cytoplasmic proteins organelles in lysosome-dependent manner, inhibited rats. Our current data confirm inhibition...
Clinical and experimental studies show that spinal cord injury (SCI) can cause cognitive impairment depression significantly impact outcomes. Thus, identifying mechanisms responsible for these less well-examined, important SCI consequences may provide targets more effective therapeutic intervention. To determine whether depressive-like changes correlate with severity, we exposed mice to sham, mild, moderate, or severe using the Infinite Horizon Spinal Cord Impactor evaluated performance on a...
Following spinal cord injury (SCI), astrocytes demonstrate long-lasting reactive changes, which are associated with the persistence of neuropathic pain and motor dysfunction. We previously demonstrated that upregulation trkB.T1, a truncated isoform brain-derived neurotrophic factor receptor (BDNF), contributes to gliosis after SCI, but little is known about effects trkB.T1 on function astrocytes. As sole trkB receptors expressed astrocytes, we examined trkB.T1-driven in vitro vivo ....
Cognitive dysfunction has been reported in patients with spinal cord injury (SCI), but it questioned whether such changes may reflect concurrent head injury, and the issue not addressed mechanistically or a well-controlled experimental model. Our recent rodent studies examining SCI-induced hyperesthesia revealed neuroinflammatory only supratentorial pain-regulatory sites, also other brain regions, suggesting that additional functions be impacted following SCI. Here we examined effects of...
Autophagy is a catabolic process that degrades cytoplasmic constituents and organelles in the lysosome, thus serving an important role cellular homeostasis protection against insults.We previously reported defects autophagy contribute to neuronal cell damage traumatic spinal cord injury (SCI).Recent data from other inflammatory models implicate regulation of immune responses, with low levels autophagic flux associated pro-inflammatory phenotypes.In present study, we examined effects...
Environmental enrichment is known to enhance hippocampal neurogenesis and cognitive functions. Neurogranin (Ng), a specific substrate of protein kinase C (PKC), abundantly expressed in brain regions important for Deletion Ng mice causes severe deficits spatial learning long-term potentiation (LTP) the CA1 region. These Ng−/− mice, as compared with Ng+/+, respond poorly after treatment their slices agents that activate signaling molecules memory, including Ca<sup>2+</sup>/calmodulin-dependent...
Paucity of permissive molecules and abundance inhibitory in the injured spinal cord adult mammals prevent axons from successful regeneration and, thus, contribute to failure functional recovery. Using an adeno-associated viral (AAV) vector, we expressed regeneration-promoting cell adhesion molecule L1 both neurons glia lesioned mice. Exogenous L1, detectable already 1 week after thoracic compression immediate vector injection, was at high levels up 5 weeks, longest time-period studied....
The Ig superfamily adhesion molecule CHL1, the close homolog of L1, promotes neurite outgrowth, neuronal migration, and survival in vitro . We tested whether similar to its has a beneficial impact on recovery from spinal cord injury using adult CHL1-deficient ( CHL1 −/− ) mice wild-type +/+ littermates. In contrast our hypothesis, we found that functional recovery, assessed by locomotor rating video-based motion analyses, was improved compared with at 3–6 weeks after compression thoracic...
Spinal cord injury (SCI) frequently causes severe, persistent central neuropathic pain that responds poorly to conventional treatments. Brain-derived neurotrophic factor (BDNF) signaling appears contribute sensitization and nocifensive behaviors in certain animal models of chronic through effects mediated part by the alternatively spliced truncated isoform BDNF receptor tropomyosin-related kinase B.T1 (trkB.T1). Mechanisms linking trkB.T1 SCI-induced are unknown. Here, we examined role after...