A transient neurodevelopmental microglial state governs cortical maturation and is disrupted by neonatal inflammation in mouse
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE337230 | GEO | 2026/07/01
REPOSITORIES: GEO
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Project description:Neonatal hypoxic-ischemic (HI) encephalopathy can lead to severe brain damage and is a common cause of neurological handicaps in adulthood. To elucidate the molecular events occurring in cerebral cortices of mature rats (8 weeks old) after neonatal HI brain insult, we performed comprehensive gene expression and gene network analyses using a DNA microarray system (Agilent 4x44K). A rat model of neonatal HI encephalopathy (Rice model) was obtained by unilateral ligation of the common carotid artery of 7-day-old rats with hypoxia (exposure to 8% oxygen). Due to the HI insult-related breakdown of the ipsilateral hemisphere in the brain, RNAs were prepared from the contralateral cerebral cortices of 8-week-old rats and analyzed by DNA microarray. Biofunctional analysis of differentially regulated genes revealed that many upregulated genes were related to cell death signaling, such as the arachidonic acid cascade. In contrast, many downregulated genes were related to gene expression, reflecting progressive damage by the HI insult, even within the contralateral cerebral hemisphere. Seven-day-old Wistar rats were assigned to two groups: the control group and the Rice group (four pups in each group). HI brain insult was not induced in the control group rats. The Rice group rats were subjected to a modified LevineM-bM-^@M-^Ys procedure to induce HI brain injury. The Rice group rats were anesthetized with ether, and the left carotid artery was sectioned between double ligatures with 4-0 surgical silk. The rats were allowed to recover for 1M-bM-^@M-^S2 h and then exposed to 1 h of hypoxia in a plastic chamber that was perfused with a mixture of humidified 8% oxygen balanced with nitrogen. The temperature inside the chamber was maintained at 33 M-BM-0C, the usual temperature generated when pups huddle with the mother. The cerebral cortexes contralateral to the HI brain insult and those of the same side of the control animals were used for the experiment.
2012-06-27 | E-GEOD-37777 | biostudies-arrayexpress
Project description:Neonatal hypoxic-ischemic (HI) encephalopathy can lead to severe brain damage and is a common cause of neurological handicaps in adulthood. To elucidate the molecular events occurring in cerebral cortices of mature rats (8 weeks old) after neonatal HI brain insult, we performed comprehensive gene expression and gene network analyses using a DNA microarray system (Agilent 4x44K). A rat model of neonatal HI encephalopathy (Rice model) was obtained by unilateral ligation of the common carotid artery of 7-day-old rats with hypoxia (exposure to 8% oxygen). Due to the HI insult-related breakdown of the ipsilateral hemisphere in the brain, RNAs were prepared from the contralateral cerebral cortices of 8-week-old rats and analyzed by DNA microarray. Biofunctional analysis of differentially regulated genes revealed that many upregulated genes were related to cell death signaling, such as the arachidonic acid cascade. In contrast, many downregulated genes were related to gene expression, reflecting progressive damage by the HI insult, even within the contralateral cerebral hemisphere.
2012-06-28 | GSE37777 | GEO
Project description: Not available
| S-EPMC10015752 | biostudies-literature
Project description:Background: Fetal hypoxia causes vital, systemic, developmental malformations in the fetus, particularly in the brain, and increases the risk of diseases in later life. We previously demonstrated that fetal hypoxia exposure increases the susceptibility of the neonatal brain to hypoxic-ischemic insult. Herein, we investigate the effect of fetal hypoxia on programming of cell-specific transcriptomes in the brain of neonatal rats.
2023-03-22 | GSE216946 | GEO
Project description:Neonatal hypoxic-ischemic (HI) encephalopathy can lead to severe brain damage, and is a common cause of neurological handicaps in adulthood. The modified Levine method (Rice model) has been widely used as an animal model of this condition, which can be rescued by the administration of an antioxidant such as 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186). In the present study, by using the Rice model, we performed comprehensive gene expression and gene network analyses of neonatal HI brain insult with and without MCI-186 administration via a DNA microarray to help elucidate the molecular events responsible for the selective vulnerability of neurons to an HI insult and the underlying mechanisms of the effect of MCI-186 on the pathophysiological events. A large difference in gene expression was observed between the Rice model and the control. By performing a clustering analysis of the gene expression pattern after the HI brain insult, we found the following 3 clusters: (i) a cluster of strongly upregulated genes mainly consisting of genes related to immune responses; (ii) a cluster of mildly upregulated genes mainly consisting of genes related to cellular movement, growth and proliferation, and cell death; and (iii) a cluster of downregulated genes mainly consisting of genes related to neuronal activity. The effect of MCI-186 administration on gene expression was much less than and contrary to that of the HI brain insult. The genes upregulated and downregulated on MCI-186 administration were closely related to neuronal activity and immune responses, respectively, thereby reflecting the protective effect of MCI-186 on an HI brain insult.
2010-03-05 | GSE18356 | GEO
Project description:The functions and protein expressions of the blood-brain barrier are changed during brain development after birth. The purpose of the present study was to develop a method to isolate brain capillaries from a single frozen neonatal mouse brain and elucidate the enrichment of brain capillaries by quantitative proteomic analysis. The brain capillary fraction was prepared by the optimized method from a single frozen mouse neonatal brain (postnatal day 7). The brain capillary fractions and brain lysates were digested by trypsin and analyzed by DIA.
| PXD039296 | JPOST Repository
Project description:Neonatal beta cells are considered developmentally immature and hence less glucose-responsive. To study the acquisition of mature glucose-responsiveness, we compared glucose-regulated redox state, insulin synthesis and secretion of beta cells purified from neonatal or 10-weeks old rats to their transcriptomes and proteomes measured by oligonucleotide and LC-MS/MS profiling. Lower glucose-responsiveness of neonatal beta cells was explained by two distinct properties: higher activity at low glucose and lower activity at high glucose. Basal hyperactivity was associated with higher NAD(P)H, a higher fraction of neonatal beta cells actively incorporating 3H-Tyrosine, and persistently increased insulin secretion below 5 mM glucose. Neonatal beta cells lacked the steep glucose-responsive NAD(P)H rise between 5-10 mM glucose characteristic for adult beta cells, and accumulated less NAD(P)H at high glucose. They had 2-fold lower expression of malate/aspartate-NADH shuttle and most glycolytic enzymes. Genome-wide profiling situated neonatal beta cells at a developmental crossroad: they showed advanced endocrine differentiation when specifically analyzed for their mRNA/protein level of classical neuroendocrine markers. On the other hand, discrete neonatal beta cell subpopulations still expressed mRNAs/proteins typical for developing/proliferating tissues. One example, Delta-like 1 homolog (DLK1) was used to investigate if neonatal beta cells with basal hyperactivity corresponded to a more immature subset with high DLK1, but no association was found. In conclusion, the current study supports the importance of glycolytic NADH-shuttling in stimulus-function coupling, presents basal hyperactivity as novel property of neonatal beta cells, and provides potential markers to recognize intercellular developmental differences in the endocrine pancreas.
2014-12-12 | PXD001577 | Pride
Project description:We search for developmental changes specific to humans by examining gene expression profiles in the human, chimpanzee and rhesus macaque prefrontal and cerebellar cortex. In both brain regions, developmental patterns were more evolved in humans than in chimpanzees. To distinguish whether the human specific developmental pattern represent novel human-specific developmental patterns or a shift in the timing of the existing patterns, we measured mRNA expression patterns in macaque brains from prenatal to neonatal. Our results show that the major human-specific developmental patterns identified in the PFC reflects an extreme shift in timing of synaptic development. Rhesus macaque post-mortem brain samples from the superior frontal gyrus region of the prefrontal cortex were collected. Six fetal and six newborn samples were used. RNA extracted from the dissected tissue was hybridized to Affymetrix® Human Gene 1.0 ST arrays.
2012-02-02 | E-GEOD-29138 | biostudies-arrayexpress
Project description:We search for developmental changes specific to humans by examining gene expression profiles in the human, chimpanzee and rhesus macaque prefrontal and cerebellar cortex. In both brain regions, developmental patterns were more evolved in humans than in chimpanzees. To distinguish whether the human specific developmental pattern represent novel human-specific developmental patterns or a shift in the timing of the existing patterns, we measured mRNA expression patterns in macaque brains from prenatal to neonatal. Our results show that the major human-specific developmental patterns identified in the PFC reflects an extreme shift in timing of synaptic development.
2012-02-02 | GSE29138 | GEO
Project description:Cy3-labeled cDNA obtained from four pools of three hearts of neonatal C57BL Cx43 null mice were compared to Cy3-labeled cDNA obtained from four pools of three hearts of neonatal C57BL wildtype mice through Cy5-labeled sample reference prepared at once for the entire experiment from aorta, brain, heart, kidney, liver, lung, ovary/testicles, spleen, and stomach - equal amounts from adult male and female C57BL mice. Keywords = Cx32 null vs wildtype neonatal mouse heart
2010-06-05 | E-GEOD-1961 | biostudies-arrayexpress