Jialing Liu

ORCID: 0000-0003-4420-4382
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroscience and Neuropharmacology Research
  • Neurological Disease Mechanisms and Treatments
  • Acute Ischemic Stroke Management
  • Cerebrovascular and Carotid Artery Diseases
  • Neural dynamics and brain function
  • Anesthesia and Neurotoxicity Research
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Neonatal and fetal brain pathology
  • Biochemical effects in animals
  • Axon Guidance and Neuronal Signaling
  • Angiogenesis and VEGF in Cancer
  • Heat shock proteins research
  • Photoacoustic and Ultrasonic Imaging
  • Mitochondrial Function and Pathology
  • Olfactory and Sensory Function Studies
  • Functional Brain Connectivity Studies
  • Moyamoya disease diagnosis and treatment
  • Alzheimer's disease research and treatments
  • Intracranial Aneurysms: Treatment and Complications
  • Stroke Rehabilitation and Recovery
  • Atherosclerosis and Cardiovascular Diseases
  • Connexins and lens biology
  • Adipokines, Inflammation, and Metabolic Diseases

University of California, San Francisco
2013-2025

San Francisco VA Medical Center
2016-2025

Neurological Surgery
2015-2025

Chifeng Municipal Hospital
2025

Inner Mongolia Medical University
2025

Beijing University of Technology
2025

Southern University of Science and Technology
2024

China People's Police University
2024

Third Affiliated Hospital of Sun Yat-sen University
2024

Sun Yat-sen University
2024

Neurogenesis in the dentate gyrus of adult rodents is regulated by NMDA receptors, adrenal steroids, environmental stimuli, and seizures. To determine whether ischemia affects neurogenesis, newly divided cells were examined after transient global gerbils. 5-Bromo-2′-deoxyuridine-5′-monophosphate (BrdU) immunohistochemistry demonstrated a 12-fold increase cell birth subgranular zone 1–2 weeks 10 min bilateral common carotid artery occlusions. Two minutes did not significantly BrdU...

10.1523/jneurosci.18-19-07768.1998 article EN cc-by-nc-sa Journal of Neuroscience 1998-10-01

GLT-1, GLAST, and EAAC1 are high-affinity, Na + -dependent glutamate transporters identified in rat forebrain. The expression of these transporter subtypes was characterized three preparations: undifferentiated cortical astrocyte cultures, astrocytes cocultured with neurons, cultures differentiated dibutyryl cyclic AMP (dBcAMP). monocultures expressed only the GLAST subtype. Astrocytes neurons developed a stellate morphology both GLT-1; transporter, rare microglia GLT-1. Treatment dBcAMP...

10.1523/jneurosci.17-03-00932.1997 article EN cc-by-nc-sa Journal of Neuroscience 1997-02-01

Marek disease virus (MDV) is a herpesvirus of chickens that induces T lymphomas within 3 weeks infection. The short latency and polyclonal nature MDV-induced tumors have suggested the may encode one or more direct-acting oncogenes. To date, however, no MDV-specific tumor antigens candidate transforming genes been demonstrated. In this paper, we report identification MDV gene encoding protein with homology to leucine-zipper class nuclear It also contains proline-rich domain characteristic...

10.1073/pnas.89.9.4042 article EN Proceedings of the National Academy of Sciences 1992-05-01

Abstract Increased neurogenesis after cerebral ischemia suggests that functional recovery stroke may be attributed, in part, to neural regeneration. In this study, we investigated the role of behavioral performance gerbils global ischemia. We used ionizing radiation decrease regeneration, and 2 weeks later was induced by bilateral common carotid artery occlusion. One month occlusion, animals were behaviorally tested. Irradiation alone reduced but did not change vascular or dendritic...

10.1002/ana.10853 article EN Annals of Neurology 2004-02-03

Severe hypoglycemia causes neuronal death and cognitive impairment. Evidence suggests that hypoglycemic involves excitotoxicity DNA damage. Poly(ADP-ribose) polymerase-1 (PARP-1) normally functions in repair, but promotes cell when extensively activated by Cortical neuron cultures were subjected to glucose deprivation assess the role of PARP-1 death. -/- neurons wild-type, +/+ treated with PARP inhibitor 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone both showed increased...

10.1523/jneurosci.23-33-10681.2003 article EN cc-by-nc-sa Journal of Neuroscience 2003-11-19

Apoptosis is implicated in neonatal hypoxic/ischemic (H/I) brain injury among various forms of cell death. Here we investigate whether overexpression heat shock protein (Hsp) 70, an antiapoptotic protein, protects the from H/I and pathways involved protection. Postnatal day 7 (P7) transgenic mice overexpressing rat Hsp70 (Tg) their wild-type littermates (Wt) underwent unilateral common carotid artery ligation followed by 30 mins exposure to 8% O(2). Significant neuroprotection was observed...

10.1038/sj.jcbfm.9600080 article EN Journal of Cerebral Blood Flow & Metabolism 2005-03-02

Traumatic brain injury (TBI) provokes inflammatory responses, including a dramatic rise in macrophages the area of injury. The pathway(s) responsible for macrophage infiltration traumatically injured and effects on functional outcomes are not well understood. C-C-chemokine receptor 2 (CCR2) is known directing monocytes to inflamed tissues. To assess role CCR2 TBI, we determined CCR2-deficient (Ccr2−/−) mice controlled cortical impact model. We quantified myeloid cell numbers post-TBI by flow...

10.1089/neu.2013.3252 article EN Journal of Neurotrauma 2014-05-08

In the adult brain, neurogenesis occurs in subgranular zone of dentate gyrus (DG), where high levels vesicular zinc are localized presynaptic terminals. To determine whether has a role modulating hippocampal under normal or pathologic conditions, we manipulated level experimentally. reduce zinc, rats were either fed zinc-deficient diet treated with chelator, clioquinol (CQ). The number progenitor cells and immature neurons was decreased significantly DG after 6 weeks dietary deprivation....

10.1038/jcbfm.2009.80 article EN Journal of Cerebral Blood Flow & Metabolism 2009-06-17

Abstract Background Traumatic brain injury (TBI) induces activation of microglia. Activated microglia can in turn increase secondary and impair recovery. This innate immune response requires hours to days become fully manifest, thus providing a clinically relevant window opportunity for therapeutic intervention. Microglial is regulated part by poly(ADP-ribose) polymerase-1 (PARP-1). Inhibition PARP-1 activity suppresses NF-kB-dependent gene transcription thereby blocks several aspects...

10.1186/1742-2094-9-31 article EN cc-by Journal of Neuroinflammation 2012-02-15

Hypoglycemia-induced brain injury is a significant obstacle to optimal blood glucose control in diabetic patients. Severe hypoglycemia triggers cascade of events vulnerable neurons that may culminate cell death even after normalization. A key event this the activation poly(ADP-ribose) polymerase-1 (PARP-1). Activated PARP-1 consumes cytosolic NAD, and because NAD required for glycolysis, hypoglycemia-induced render cells unable use when availability restored. Pyruvate, however, can be...

10.2337/diabetes.54.5.1452 article EN Diabetes 2005-05-01

Abstract Radiation therapy is a widely used treatment for brain tumors but it can cause delayed progressive cognitive decline and memory deficits. Previous studies suggested that this neurocognitive dysfunction might be linked to the impairment of hippocampal neurogenesis. However, little known regarding how reduce caused by radiation therapy. To investigate whether environmental enrichment (EE) promotes neurogenesis function after irradiation, irradiated gerbils were housed in EE 2 months...

10.1111/j.1460-9568.2006.05269.x article EN European Journal of Neuroscience 2007-01-01

The selective serotonin reuptake inhibitor fluoxetine induces hippocampal neurogenesis, stimulates maturation and synaptic plasticity of adult neurons, reduces motor/sensory memory impairments in several CNS disorders. In the setting traumatic brain injury (TBI), its effects on neuroplasticity function have yet to be thoroughly investigated. Here we examined efficacy after a moderate severe TBI, produced by controlled cortical impact. Three days TBI or sham surgery, mice were treated with...

10.1089/neu.2010.1648 article EN Journal of Neurotrauma 2010-12-22

Abstract Background Recurrent/moderate (R/M) hypoglycemia is common in type 1 diabetes. Although mild or moderate not life-threatening, if recurrent, it may cause cognitive impairment. In the present study, we sought to determine whether R/M leads neuronal death, dendritic injury, Methods The experiments were conducted normal and diabetic rats. Rats subjected by insulin without anesthesia. Oxidative stress was evaluated 4-Hydroxy-2-nonenal immunostaining death determined Fluoro-Jade B...

10.1186/1742-2094-9-182 article EN cc-by Journal of Neuroinflammation 2012-07-25

The causal relationship between neurogenesis and the recovery of poststroke cognitive function has not been properly explored. current study aimed to determine whether depleting neuroprogenitor cells (NPCs) affects functional outcome in nestin-δ-HSV-TK-EGFP transgenic mice, which expression a truncated viral thymidine kinase gene EGFP was restricted nestin-expressing NPCs. Ganciclovir (GCV; 200 mg/kg/d) or saline continuously administered via osmotic pumps mice for 4 weeks before induction...

10.1523/jneurosci.2129-13.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-10-30

Collateral status is an independent predictor of stroke outcome. However, the spatiotemporal manner in which collateral flow maintains cerebral perfusion during ischemia poorly understood. Diabetes exacerbates ischemic brain damage, although impact diabetes on dynamics remains to be established. Using Doppler optical coherent tomography, a robust recruitment leptomeningeal was detected immediately after middle artery (MCA) occlusion C57BL/6 mice, and it continued grow over course 1 week. In...

10.1523/jneurosci.3838-14.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-03-04

Triggering receptor expressed on myeloid cells-2 (TREM2) is an innate immune that promotes phagocytosis by cells such as microglia and macrophages. We previously showed TREM2 deficiency worsened outcomes from experimental stroke impeded phagocytosis. However, participating in pathology include both brain resident circulating now clarify whether or macrophages contribute to its beneficial role ischemic generating bone marrow (BM) chimeric mice. BM chimera mice knockout (KO) wild type (Wt)...

10.1177/0271678x18817282 article EN Journal of Cerebral Blood Flow & Metabolism 2018-12-07
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