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A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE275713 | GEO | 2024/10/02

REPOSITORIES: GEO

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A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes [bulkRNA-seq]

Project description:Neonatal hypoxic ischemic encephalopathy (HIE) occurs in 1.5 per 1000 live births, leaving affected children with long-term motor and cognitive deficits. Few animal models of HIE incorporate maternal immune activation (MIA) despite the significant risk MIA poses to HIE incidence and diagnosis. Our non-invasive model of HIE pairs late gestation MIA with postnatal hypoxia. HIE pups exhibited a trend toward smaller overall brain size and delays in the ontogeny of several developmental milestones. In adulthood, HIE animals had reduced strength and gait deficits, but no difference in speed. Surprisingly, HIE animals performed better on the rotarod, an assessment of motor coordination. There was significant upregulation of inflammatory genes in microglia 24 hours after hypoxia, which were largely downregulated one week later. Single cell RNAseq revealed upregulation of epigenetic machinery in macrophages invading the brain following HIE. These results support a two-hit noninvasive model pairing MIA and hypoxia as a model for HIE in humans. This model results in a mild phenotype compared to established HIE models; however, HIE is a clinically heterogeneous injury resulting in a variety of outcomes in humans. The pathways identified in our model of HIE may yield novel targets for therapy for neonates with HIE.

2024-10-02 | GSE275712 | GEO

A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes [scRNA-seq]

2024-10-02 | GSE274183 | GEO

A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes

Project description:A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes

| PRJNA1152600 | ENA

A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes [bulkRNA-seq]

| PRJNA1152603 | ENA

A novel noninvasive murine model of neonatal hypoxic ischemic encephalopathy demonstrates developmental delay and motor deficits with activation of inflammatory pathways in monocytes [scRNA-seq]

| PRJNA1145365 | ENA

Neuroprotective Strategies after Neonatal Hypoxic Ischemic Encephalopathy.

Project description:Neonatal hypoxic ischemic encephalopathy (HIE) is a devastating disease that primarily causes neuronal and white matter injury and is among the leading cause of death among infants. Currently there are no well-established treatments; thus, it is important to understand the pathophysiology of the disease and elucidate complications that are creating a gap between basic science and clinical translation. In the development of neuroprotective strategies and translation of experimental results in HIE, there are many limitations and challenges to master based on an appropriate study design, drug delivery properties, dosage, and use in neonates. We will identify understudied targets after HIE, as well as neuroprotective molecules that bring hope to future treatments such as melatonin, topiramate, xenon, interferon-beta, stem cell transplantation. This review will also discuss some of the most recent trials being conducted in the clinical setting and evaluate what directions are needed in the future.

| S-EPMC4613313 | biostudies-literature

Language in children with neonatal hypoxic-ischemic encephalopathy.

Project description:Introduction Neonatal hypoxic-ischemic encephalopathy (NHIE) is a common neurologic injury, and it may compromise the child's language and cognition. Understanding the process of language acquisition becomes possible with concise knowledge about children's global development. Objective The aim of this study was to observe if language acquisition and development are impaired in children with NHIE. Methods Seventy children with NHIE from 1 to 24 months old were analyzed in a Pediatric Neurology Service of Hospital of Porto Alegre, South of Brazil using the Brunet-Lezine Scale. Statistical analysis used SPSS 13.0 software. Results Twenty-four (60%) of the subjects were boys, with mean gestational age of 35.8 weeks (standard deviation of 4.6) and mean Apgar score of 6.0 at 1 minute and 7.1 at 5 minutes. The variables age versus language showed significant inverse correlation (r = - 0.566; p = 0.028). As the subjects aged, language tasks became more specific and dependent on the subject's direct action, rather than the subjective interpretation of their guardian. This correlation seems to be closely associated with scale configuration and with consequences of neurologic disorder, evincing the delays in language development. Conclusion This study achieved the goals proposed and highlights the necessity of greater attention by professionals to language skills during the initial period of child development.

| S-EPMC4297029 | biostudies-other

Vitamin D insufficiency in neonatal hypoxic-ischemic encephalopathy.

Project description:BACKGROUND:Vitamin D has neuroprotective and immunomodulatory properties, and deficiency is associated with worse stroke outcomes. Little is known about effects of hypoxia-ischemia or hypothermia treatment on vitamin D status in neonates with hypoxic-ischemic encephalopathy (HIE). We hypothesized vitamin D metabolism would be dysregulated in neonatal HIE altering specific cytokines involved in Th17 activation, which might be mitigated by hypothermia. METHODS:We analyzed short-term relationships between 25(OH) and 1,25(OH)2 vitamin D, vitamin D binding protein, and cytokines related to Th17 function in serum samples from a multicenter randomized controlled trial of hypothermia 33 °C for 48?h after HIE birth vs. normothermia in 50 infants with moderate to severe HIE. RESULTS:Insufficiency of 25(OH) vitamin D was observed after birth in 70% of infants, with further decline over the first 72?h, regardless of treatment. 25(OH) vitamin D positively correlated with anti-inflammatory cytokine IL-17E in all HIE infants. However, Th17 cytokine suppressor IL-27 was significantly increased by hypothermia, negating the IL-27 correlation with vitamin D observed in normothermic HIE infants. CONCLUSION:Serum 25(OH) vitamin D insufficiency is present in the majority of term HIE neonates and is related to lower circulating anti-inflammatory IL-17E. Hypothermia does not mitigate vitamin D deficiency in HIE.

| S-EPMC5509506 | biostudies-literature

Evolution of encephalopathy during whole body hypothermia for neonatal hypoxic-ischemic encephalopathy.

Project description:To examine the predictive ability of stage of hypoxic-ischemic encephalopathy (HIE) for death or moderate/severe disability at 18 months among neonates undergoing hypothermia.Stage of encephalopathy was evaluated at <6 hours of age, during study intervention, and at discharge among 204 participants in the National Institute of Child Health and Human Development Neonatal Research Network Trial of whole body hypothermia for HIE. HIE was examined as a predictor of outcome by regression models.Moderate and severe HIE occurred at <6 hours of age among 68% and 32% of 101 hypothermia group infants and 60% and 40% of 103 control group infants, respectively. At 24 and 48 hours of study intervention, infants in the hypothermia group had less severe HIE than infants in the control group. Persistence of severe HIE at 72 hours increased the risk of death or disability after controlling for treatment group. The discharge exam improved the predictive value of stage of HIE at <6 hours for death/disability.On serial neurologic examinations, improvement in stage of HIE was associated with cooling. Persistence of severe HIE at 72 hours and an abnormal neurologic exam at discharge were associated with a greater risk of death or disability.

| S-EPMC3299861 | biostudies-other

Different antecedents and neonatal condition in neonatal arterial ischemic stroke and hypoxic-ischemic neonatal encephalopathy.

Project description:ObjectiveTo define similarities and differences between neonatal arterial ischemic stroke (NAIS) and hypoxic-ischemic neonatal encephalopathy (HINE).MethodsA retrospective case-control study was conducted of neonates born at 35 weeks or more and weighing 1800 g or more at a tertiary care university hospital, between 2005 and 2016, with NAIS (group A), perinatal asphyxia (PA) with Stage II-III HINE (group B), and PA with or without Stage I HINE (group C). Ante- and intrapartum data, neonatal characteristics, and placental histopathology were compared.ResultsEleven neonates were identified in group A, 10 in group B, and 227 in group C. Sentinel events occurred exclusively in groups B (80%) and C (41.4%). Umbilical cord blood gas values and Apgar score were worse in groups B and C compared to group A. No group A neonates required resuscitation at birth, whereas all group B and one-third of group C neonates did. Seizures developed only in neonates in groups A and B. One neonatal death occurred in group A. There were no significant differences in placental histopathology.ConclusionNAIS and PA/HINE cases have different intrapartum and neonatal features. PA does not seem necessary for the occurrence of NAIS. More research is needed regarding associated placental abnormalities.

| S-EPMC9290624 | biostudies-literature

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