Julien Pansiot

ORCID: 0000-0002-3518-3973
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About
Contact & Profiles
Research Areas
  • Neonatal and fetal brain pathology
  • Neonatal Respiratory Health Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Birth, Development, and Health
  • Anesthesia and Neurotoxicity Research
  • Pregnancy and preeclampsia studies
  • Infant Development and Preterm Care
  • Immune Response and Inflammation
  • Nitric Oxide and Endothelin Effects
  • Adenosine and Purinergic Signaling
  • Neuroscience of respiration and sleep
  • Phosphodiesterase function and regulation
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Stress Responses and Cortisol
  • S100 Proteins and Annexins
  • Inflammatory mediators and NSAID effects
  • Congenital Diaphragmatic Hernia Studies
  • Neuroendocrine regulation and behavior
  • Neonatal and Maternal Infections
  • Neuroscience and Neuropharmacology Research
  • Infant Nutrition and Health
  • Advanced Vision and Imaging
  • Estrogen and related hormone effects
  • Human Pose and Action Recognition
  • Reproductive System and Pregnancy

Inserm
2014-2025

Université Paris Cité
2014-2025

NeuroDiderot
2015-2025

Délégation Paris 7
2014-2025

Centre Inria de l'Université Grenoble Alpes
2023

Institut national de recherche en informatique et en automatique
2023

Sorbonne Paris Cité
2012-2021

Hôpital Robert-Debré
2009-2020

Sorbonne Université
2010-2018

PremUP
2009-2017

Preterm birth places infants in an adverse environment that leads to abnormal brain development and cerebral injury through a poorly understood mechanism known involve neuroinflammation. In this study, we integrate human mouse molecular neuroimaging data investigate the role of microglia preterm white matter damage. Using model where encephalopathy prematurity is induced by systemic interleukin-1β administration, undertake gene network analysis microglial transcriptomic response injury,...

10.1038/s41467-017-00422-w article EN cc-by Nature Communications 2017-08-30

Objective To investigate the effects of melatonin treatment in a rat model white matter damage (WMD) developing brain. Additionally, we aim to delineate cellular mechanisms effect on oligodendroglial cell lineage. Methods A unilateral ligation uterine artery pregnant at embryonic day 17 induces fetal hypoxia and subsequent growth restriction (GR) neonatal pups. GR control pups received daily intra-peritoneal injection from birth post-natal (P) 3. Results Melatonin administration was...

10.1371/journal.pone.0007128 article EN cc-by PLoS ONE 2009-09-21

The cognitive and behavioural deficits caused by traumatic brain injury (TBI) to the immature are more severe persistent than TBI in mature brain. Understanding this developmental sensitivity is critical as children under four years of age sustain frequently any other group. Microglia (MG), resident immune cells that mediate neuroinflammation, activated following However, type temporal profile activation consequences altering it still largely unknown. In a mouse model closed head weight drop...

10.1016/j.bbi.2016.11.001 article EN cc-by Brain Behavior and Immunity 2016-11-04

Abstract Prematurity and fetal growth restriction (FGR) are frequent conditions associated with adverse neurocognitive outcomes. We have previously identified early deregulation of genes controlling neuroinflammation as a putative mechanism linking FGR abnormal trajectory the developing brain. While oxytocin system was also found to be impaired following perinatal events, its role in modulation brain is still unknown. used double‐hit rat model injury induced by gestational low protein diet...

10.1002/glia.23546 article EN Glia 2018-12-02

Fetal growth restriction (FGR) is a major complication of human pregnancy, frequently resulting from placental vascular diseases and prenatal malnutrition, associated with adverse neurocognitive outcomes throughout life. However, the mechanisms linking poor fetal impairment are unclear. Here, we aimed to correlate changes in gene expression induced by FGR rats abnormal cerebral white matter maturation, brain microstructure, cortical connectivity vivo. We investigated model low-protein-diet...

10.1002/glia.23079 article EN Glia 2016-09-30

Neuroinflammation has a key role in the pathogenesis of perinatal brain injury. Caffeine, nonspecific antagonist adenosine receptors (ARs), is widely used to treat apnea prematurity and been linked decrease incidence cerebral palsy premature infants. The mechanisms explaining its neuroprotective effect have not yet elucidated. objective this study was characterize expression ARs two neonatal rat models neuroinflammation determine A2aR blockade on microglial activation assessed through...

10.3389/fneur.2018.00605 article EN cc-by Frontiers in Neurology 2018-09-11

Background and Purpose— The best conceivable treatment for hypoxia-ischemia (HI) is the restoration of blood flow to hypoxic-ischemic region(s). Our objective was examine whether boosting NO-cGMP signaling using sildenafil citrate, a phosphodiesterase-type 5 inhibitor, could modify cerebral reduce lesions in developing brain. Methods— HI induced P7 Sprague–Dawley rats by unilateral carotid artery occlusion hypoxia, followed either PBS or sildenafil. Blood-flow velocities were measured...

10.1161/strokeaha.113.003606 article EN Stroke 2014-01-29

Perinatal ischemic stroke is the most frequent form of cerebral infarction in neonates; however, evidence-based treatments are currently lacking. We have previously demonstrated a beneficial effect sildenafil citrate, PDE-5 inhibitor, on lesion size neonatal rat pups. The present study investigated effects mouse model (1) hemodynamic changes and (2) regulation astrocyte/microglia-mediated neuroinflammation.Ischemia was induced C57Bl/6 mice postnatal (P) day 9 by permanent middle artery...

10.1186/s12974-016-0560-4 article EN cc-by Journal of Neuroinflammation 2016-04-28

Abstract Background and purpose The only validated treatment to prevent brain damage associated with hypoxia–ischemia (HI) encephalopathy of the newborn is controlled hypothermia limited benefits. Additional putative neuroprotective drug candidates include sildenafil citrate, a phosphodiesterase-type 5 inhibitor. main objective this preclinical study assess its ability reduce HI-induced neuroinflammation, in particular through potential effect on microglial activation. Methods HI was induced...

10.1186/s12974-024-03022-w article EN cc-by Journal of Neuroinflammation 2024-01-23

Metabotropic glutamate (mGlu) receptors are candidate drug targets for therapeutic intervention in Parkinson's disease (PD). Here we focused on mGlu3, a receptor subtype involved synaptic regulation and neuroinflammation. mGlu3−/− mice showed an enhanced nigro-striatal damage microglial activation response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Expression of genes encoding anti-inflammatory proteins neuroprotective factors was reduced the striatum MPTP-treated mice. We also...

10.1038/s41531-024-00860-6 article EN cc-by-nc-nd npj Parkinson s Disease 2025-01-04

Perinatal brain injury including white matter damage (WMD) is highly related to sensory, motor or cognitive impairments in humans born prematurely. Our aim was examine the neuroanatomical, functional and behavioral changes adult rats that experienced prenatal ischemia (PI), thereby inducing WMD. PI induced by unilateral uterine artery ligation at E17 pregnant rats. We assessed performances gait, abilities topographical organization of maps, neuronal glial density primary somatosensory...

10.1111/j.1750-3639.2011.00504.x article EN Brain Pathology 2011-05-26

Background Inhaled nitric oxide (iNO) is one of the most promising therapies used in neonates. However, little information known about its impact on developing brain submitted to excitotoxic challenge. Methodology/Principal Findings We investigated here effect iNO a neonatal model lesions. Rat pups and their dams were placed chamber containing 20 ppm NO during first week life. At postnatal day (P)5, rat intracranial injection glutamate agonists. P10, exposed exhibited significant decrease...

10.1371/journal.pone.0010916 article EN cc-by PLoS ONE 2010-06-01

White matter damage (WMD) remains the leading cause of cerebral palsy in children born prematurely. The release an excessive amount reactive oxygen species is recognized as a risk factor for WMD. We hypothesize that free radical injury during reoxygenation at birth may be harmful to immature white and underlie, least part, pathogenesis tested this hypothesis rat pups delivered from normoxic pregnant rats, by investigating animal model based on protracted antenatal hypoxia mimicking main...

10.1159/000327245 article EN Developmental Neuroscience 2011-01-01

Cerebral palsy (CP) is the most frequent neurological disorder associated with perinatal injury of developing brain. Major brain lesions CP are white matter damage (WMD) in preterm infants and cortico-subcortical term newborns. Cell therapy considered promising for repair damage. Human umbilical cord blood mononuclear cells (hUCB-MNCs) a rich source various stem that could be interest repairing Our goal was to investigate potential hUCB-MNCs prevent or an animal model excitotoxic injury. We...

10.1089/scd.2012.0183 article EN Stem Cells and Development 2012-05-24

Abstract Background Perinatal inflammation is a key factor of brain vulnerability in neonates born preterm or with intra-uterine growth restriction (IUGR), two leading conditions associated injury and responsible for neurocognitive behavioral disorders. Systemic recognized to activate microglia, known be the critical modulators vulnerability. Although some evidence supports role metabotropic glutamate receptor 3 (mGlu3 receptor) modulation neuroinflammation, its functions are still unknown...

10.1186/s12974-020-02049-z article EN cc-by Journal of Neuroinflammation 2021-01-06

Inhaled nitric oxide (iNO) is one of the most promising therapies used in neonates, but there little information available about its effect on developing brain. We explored effects both iNO and endogenous NO white matter rodents. Rat or mouse pups their mothers were placed a chamber containing 5 to 20 ppm for 7 days after birth. Neonatal exposure was associated with transient increase central nervous system myelination rats C57BL/6 mice without any deleterious at low doses (5 ppm) behavioral...

10.1097/nen.0b013e3181ea5203 article EN Journal of Neuropathology & Experimental Neurology 2010-07-07

The cognitive and behavioral deficits caused by traumatic brain injury (TBI) to the immature are more severe persistent than injuries adult brain. Understanding this developmental sensitivity is critical because children under 4 years of age sustain TBI frequently any other group. One first events after infiltration degranulation mast cells (MCs) in brain, releasing a range immunomodulatory substances; inhibition these neuroprotective types neonatal injury. This study investigates for time...

10.1002/jnr.23911 article EN Journal of Neuroscience Research 2016-09-10

Abstract Objective Perinatal infections and the systemic inflammatory response to them are critical contributors white matter disease (WMD) in developing brain despite use of highly active antibiotics. Fluoroquinolones including ciprofloxacin (CIP) have intrinsic anti‐inflammatory effects. We hypothesized that CIP, addition its antibacterial activity, could exert a neuroprotective effect by modulating inflammation sepsis. Methods adapted an Escherichia coli sepsis model 5‐day‐old rat pups...

10.1002/ana.22190 article EN Annals of Neurology 2010-10-27

Inhaled nitric oxide (iNO) is a therapy used in neonates with pulmonary hypertension. Some evidence of its neuroprotective properties has been reported both mature and immature brains subjected to injury. NO key mediator the VEGF pathway, angiogenesis may be involved reduced vulnerability injury white matter cortex conferred by iNO. Here, we report effect iNO on developing brain potential effectors. We found that promotes during critical window P14 rat pups. This shift developmental program...

10.3390/ijms24065871 article EN International Journal of Molecular Sciences 2023-03-20
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