- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Mitochondrial Function and Pathology
- Heat shock proteins research
- Biochemical effects in animals
- MicroRNA in disease regulation
- Anesthesia and Neurotoxicity Research
- Neurogenesis and neuroplasticity mechanisms
- Cell death mechanisms and regulation
- Endoplasmic Reticulum Stress and Disease
- Traumatic Brain Injury and Neurovascular Disturbances
- Immune Response and Inflammation
- Circular RNAs in diseases
- RNA Interference and Gene Delivery
- Cardiac Ischemia and Reperfusion
- Neonatal and fetal brain pathology
- Thermal Regulation in Medicine
- Barrier Structure and Function Studies
- Intensive Care Unit Cognitive Disorders
- Immune cells in cancer
- Neurological Disease Mechanisms and Treatments
- interferon and immune responses
- Spaceflight effects on biology
- Ion channel regulation and function
- Cardiac Arrest and Resuscitation
Stanford University
2011-2021
Stanford Medicine
1997-2019
Renmin Hospital of Wuhan University
2015
Westfield State University
2015
Wuhan University
2015
AfaSci (United States)
2011-2013
Kanazawa University
2013
Zhejiang University
2013
CACI International (United States)
2013
Northwestern University
2011
Reactive astrogliosis is characterized by a profound change in astrocyte phenotype response to all CNS injuries and diseases. To better understand the reactive state, we used Affymetrix GeneChip arrays profile gene expression populations of astrocytes isolated at various time points after induction using two mouse injury models, ischemic stroke neuroinflammation. We find gliosis consists rapid, but quickly attenuated, insult identify induced Lcn2 Serpina3n as strong markers astrocytes....
The acidosis which accompanies cerebral ischemia in vivo has been thought to contribute subsequent neuronal injury. However, recent electrophysiological recordings from hippocampal neurons suggest that H+ can attenuateN-methyl-d-aspartate (NMDA) receptor-mediated cation influx, likely a key event the pathogenesis of ischemic Here we report moderate extracellular (pH 6.5) markedly reduced inward whole cell current induced by NMDA on cultured cortical neurons; at pH 6.1, kainate-induced was...
Background— Blood–brain barrier (BBB) disruption after stroke can worsen ischemic injury by increasing edema and causing hemorrhage. We determined the effect of microglia on BBB its primary constituents, endothelial cells (ECs) astrocytes, ischemia using in vivo vitro models. Methods Results— Primary ECs, or cocultures were prepared with without added microglia. ECs more resistant to oxygen-glucose deprivation/reperfusion than astrocytes. plus astrocytes showed intermediate vulnerability....
Transient global ischemia, as with cardiac arrest, causes loss of CA1 hippocampal neurons 2–4 d later, whereas nearby dentate gyrus (DG) are relatively resistant. Whether differential astrocyte vulnerability in ischemic injury contributes to neuronal death is uncertain. Here, we find that astrocytes more sensitive ischemia than DG astrocytes. In rats subjected transient forebrain lose glutamate transport activity and immunoreactivity for GFAP, S100β, transporter GLT-1 within a few hours...
We have developed “pure” neuronal cultures (< 1% astrocytes) from mouse neocortex to study the effect of glial cells on response neurons injury. Cortical were found require glial-conditioned medium survive. Immature neurons, 2–4 d in vitro, deprived glial- conditioned medium, underwent apoptosis over 48 hr, as suggested by condensed nuclear morphology, DNA fragmentation, and protection inhibition macromolecular synthesis. Apoptosis induced trophic factor deprivation has been described for...
Recent experimental work has shown that hypothermia with even small decreases in temperature is broadly neuroprotective, but the mechanism of this protection remains unclear. Although reduction metabolism could explain by deep hypothermia, it does not robust found mild hypothermia. Several reports have suggested ischemic apoptosis reduced The authors examined effects on neuronal using serum deprivation, a well-accepted model induces apoptosis. Mild (33°C) significantly number morphologically...
Glutamate antagonists protect neurons from hypoxic injury both in vivo and vitro, but vitro studies have not been done under the acidic conditions typical of hypoxia-ischemia vivo. Consistent with glutamate receptor antagonism, extracellular acidity reduced neuronal death murine cortical cultures that were deprived oxygen glucose. Under these acid conditions, N -methyl-D-aspartate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-kainate further death, such some tolerated prolonged glucose...
Recent studies suggest a link between mitochondria and proinflammatory cytokine generation. We previously demonstrated that overexpression of mitochondrial chaperone glucose-regulated protein75 (Grp75/mortalin) protects mitochondria. In this study we investigated the modulation lipopolisaccharide (LPS)-induced inflammatory response microglial BV-2 cells by Grp75. demonstrate LPS-induced activation promotes significant metabolic changes suppressing function increasing glycolysis....
Mild hypothermia is neuroprotective, but the reasons are not well known. Inflammation contributes to ischemic damage; therefore, we examined whether protection by may be attributable alterations in inflammation. We might alter inflammatory cell-associated inducible nitric oxide synthase (iNOS) and subsequent (NO) peroxynitrite generation experimental stroke Rats underwent 2 hr of middle cerebral artery occlusion (MCAO). Brain inflammation was modeled intravenous lipopolysaccharide (LPS) (2...
Stroke causes brain injury with activation of an inflammatory response that can contribute to injury. We tested the hypothesis anti-inflammatory cytokine interleukin-4 (IL-4) reduces after stroke using IL-4 knockout (KO) adult male mice.IL-4 KO and wild-type mice were subjected transient middle cerebral artery occlusion. Outcome was assessed by triphenyltetrazolium chloride staining for infarct volume, neuroscore spontaneous activity behavioral outcome, immunostaining stereological counting...
Abstract Background We previously showed that microglia damage blood brain barrier (BBB) components following ischemic insults, but the underlying mechanism(s) is/are not well known. Recent work has established contribution of toll-like receptor 4 (TLR4) activation to several pathologies including ischemia, neurodegeneration and sepsis. The present study requirement for lipopolysaccharide (LPS) mediated endothelial cell death, explored pathways involved in this toxicity. LPS is a classic...
Mitochondria are known to be central the cell's response ischemia, because of their role in energy generation, free radical and regulation apoptosis. Heat shock protein 75 (Hsp75/Grp75/mortalin/TRAP1) is a member HSP70 chaperone family, which targeted mitochondria. Overexpression Hsp75 was achieved rat brain by DNA transfection, expression observed both astrocytes neurons. Rats were subjected 100 mins middle cerebral artery occlusion followed assessment infarct volume, neurological score,...
MicroRNA (miRNA), miR-181a, is enriched in the brain, and inhibition of miR-181a reduced astrocyte death vitro infarct volume after stroke vivo. This study investigated role neuronal injury hippocampal loss vivo forebrain ischemia. levels were altered by transfection with mimic or antagomir. N2a cells subjected to serum deprivation oxidative stress showed less cell when was increased increased; protection associated Bcl-2 protein. In contrast, transfected primary neurons did not show...
Following transient forebrain ischemia, astrocytes play a key role in determining whether or not neurons the hippocampal CA1 sector go on to die delayed fashion. MicroRNAs (miRNAs) are novel class of RNAs that control gene expression at post‐transcriptional level and miR‐29 family is highly expressed astrocytes. In this study we assessed levels hippocampus following ischemia found after short periods reperfusion, miR‐29a significantly increased resistant dentate gyrus, but decreased...