A5018499879- Pluripotent Stem Cells Research
- Immune Response and Inflammation
- CRISPR and Genetic Engineering
- Traumatic Brain Injury and Neurovascular Disturbances
- Neurogenesis and neuroplasticity mechanisms
- Phagocytosis and Immune Regulation
- Renal and related cancers
- 3D Printing in Biomedical Research
- S100 Proteins and Annexins
- Cancer-related molecular mechanisms research
- Epigenetics and DNA Methylation
- Angiogenesis and VEGF in Cancer
- Connexins and lens biology
- Cardiac Arrest and Resuscitation
- Barrier Structure and Function Studies
- Heart Rate Variability and Autonomic Control
- Alzheimer's disease research and treatments
- Inflammasome and immune disorders
- Neonatal and fetal brain pathology
- Heat shock proteins research
- interferon and immune responses
- NF-κB Signaling Pathways
- Tissue Engineering and Regenerative Medicine
- Axon Guidance and Neuronal Signaling
- Heme Oxygenase-1 and Carbon Monoxide
Virginia Tech
2017-2023
Stanford University
2018-2021
Virginia–Maryland College of Veterinary Medicine
2016-2017
Harvard Stem Cell Institute
2014
Traumatic brain injury (TBI) elicits the immediate production of proinflammatory cytokines which participate in regulating immune response. While mechanisms adaptive immunity secondary are well characterized, role innate response is unclear. Recently, NLR inflammasome has been shown to become activated following TBI, causing processing and release interleukin-1 β (IL-1 ). The a multiprotein complex consisting nucleotide-binding domain leucine-rich repeat containing proteins (NLR), caspase-1,...
Abstract Traumatic and nontraumatic brain injury results from severe disruptions in the cellular microenvironment leading to massive loss of neuronal populations increased neuroinflammation. The progressive cascade secondary events, including ischemia, inflammation, excitotoxicity, free-radical release, contribute neural tissue damage. NLRX1 is a member NLR family pattern recognition receptors potent negative regulator several pathways that significantly modulate many these events. Thus, we...
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,...
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...
Copy number variation (CNV) at the 16p11.2 locus is associated with neuropsychiatric disorders, such as autism spectrum disorder and schizophrenia. CNVs of 16p gene can manifest in opposing head sizes. Carriers deletion tend to have macrocephaly (or brain enlargement), while those duplication frequently microcephaly. Increases both gray white matter volume been observed imaging studies carriers macrocephaly. Here, we use human induced pluripotent stem cells (hiPSCs) derived from controls...
The propensity for differentiation varies substantially across human pluripotent stem cell (hPSC) lines, greatly restricting the use of hPSCs replacement therapy or disease modeling. Here, we investigate underlying mechanisms and demonstrate that activation retinoblastoma (Rb) pathway in a transient manner is important differentiation. In prior work, demonstrated pre-treating with dimethylsulfoxide (DMSO) before directed enhanced potential all three germ layers. show exposure to DMSO...
Restoration of learning and memory deficits following traumatic brain injury (TBI) is attributed, in part, to enhanced neural stem/progenitor cell (NSPCs) function. Recent findings suggest gap junction (GJ)-associated connexin 43 (Cx43) plays a key role the cycle regulation function NSPCs modulated TBI. Here, we demonstrate that Cx43 up-regulated dentate gyrus TBI expressed on vimentin-positive cells subgranular zone. To test NSPCs, exposed primary cultures α-connexin Carboxyl Terminal...
The peripheral immune system is a major regulator of the pathophysiology associated with traumatic brain injury (TBI). While age-at-injury influences recovery from TBI, differential effects on response remain unknown. Here, we investigated TBI gene expression changes in murine whole blood using RNAseq analysis, ontology and network topology-based key driver analysis. Genome-wide comparison CCI-injured showed significant increase genes involved proteolysis oxidative-reduction processes...
In Alzheimer's disease (AD) and other neurodegenerative disorders, oligodendroglial failure is a common early pathological feature, but how it contributes to development progression, particularly in the gray matter of brain, remains largely unknown. The dysfunction oligodendrocyte lineage cells hallmarked by deficiencies myelination impaired self-renewal precursor (OPCs). These two defects are caused at least part disruption interactions between neuron oligodendrocytes along buildup...
Despite the growing use of pluripotent stem cells (PSCs), challenges in efficiently differentiating embryonic and induced (ESCs iPSCs) across various lineages remain. Numerous differentiation protocols have been developed, yet variability cell lines low rates impart successfully implementing these protocols. Described here is an easy inexpensive means to enhance capacity PSCs. It has previously shown that treatment with a concentration dimethyl sulfoxide (DMSO) significantly increases...
Abstract Mechanical trauma to the CNS results in disruption of cellular microenvironment leading massive necrotic and apoptotic loss neuronal glia populations. The progressive cascade secondary events, including ischemia, inflammation, excitotoxicity free radial release contribute neural tissue damage. Members NLR family pattern recognition receptors are essential mediators host immune response. Recently, our lab others identified a novel sub-group NLRs that function as negative regulators...
Despite the growing use of pluripotent stem cells (PSCs), challenges in efficiently differentiating embryonic and induced (ESCs iPSCs) across various lineages remain. Numerous differentiation protocols have been developed, yet variability cell lines low rates impart successfully implementing these protocols. Described here is an easy inexpensive means to enhance capacity PSCs. It has previously shown that treatment with a concentration dimethyl sulfoxide (DMSO) significantly increases...
In Alzheimer's disease (AD) and other neurodegenerative disorders, oligodendroglial failure is a common early pathological feature, but how it contributes to development progression, particularly in the gray matter of brain, remains largely unknown. The dysfunction oligodendrocyte lineage cells hallmarked by deficiencies myelination impaired self-renewal precursor (OPCs). These two defects are caused at least part disruption interactions between neuron oligodendrocytes along buildup...
Abstract One of the most common genetic linkages associated with neuropsychiatric disorders, such as autism spectrum disorder and schizophrenia, occurs at 16p11.2 locus. Copy number variants (CNVs) 16p gene can manifest in opposing head sizes. deletion carriers tend to have macrocephaly (or brain enlargement), while those duplication frequently microcephaly. Increases both gray white matter volume been observed imaging studies macrocephaly. Here, we use human induced pluripotent stem cells...