Analysis of long noncoding RNA expression profile in the whole blood of neonatal Hypoxic Ischemic Encephalopathy
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PROVIDER: PRJNA496020 | ENA |
REPOSITORIES: ENA
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Project description:Long noncoding RNAs (lncRNA) have been proved to participate in many biological processes. To investigate the expression profile of lncRNAs and their potential functions in neonatal hypoxic ischemic encephalopathy (HIE). We detected the lncRNA and mRNA expression in the peripheral blood samples in HIE and relative control using microarray. A total of 376 lncRNAs and 126 mRNAs were detected to be differentially expressed between HIE and the non-HIE samples (fold change>2). Quantitative real-time PCR were used to validation of microarray data. Gene ontology (GO) enrichment and KEGG pathway analysis were used to determine the gene function. Furthermore, the co-expression network of lncRNA-mRNA were conducted to predicted the potential the targets of lncRNAs. In conclusion, our study first demonstrated the differentially expression profile of lncRNAs in the whole blood of neonatal HIE and may provide a new view of distinct lncRNAs functions in HIE.
2019-11-05 | GSE121178 | GEO
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:Hypoxic ischemic encephalopathy (HIE) is a primary cause of neonatal death and disabilities resulting from perinatal hypoxia. The progression of HI injury is closely associated with neuroinflammation. Therefore, suppressing inflammatory pathways is a promising therapeutic strategy for treating HIE. Echinatin (Ech) is a principal active component of glycyrrhiza, with anti-inflammatory and anti-oxidative effects, often combined with other herbs to exert effects of clearing heat and detoxifying. This study aimed to investigate the anti-inflammatory and neuroprotective effects of Ech on neonatal rats with hypoxic-ischemic brain damage and on PC12 cells induced by oxygen-glucose deprivation (OGD).
2024-05-07 | GSE266886 | GEO
Project description:Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.
2022-09-27 | GSE205142 | GEO
Project description:CurrentNeonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.
2022-09-27 | GSE205143 | GEO
Project description:We report the miRNA-Seq and Nanostring mRNA data from regional brain samples after neonatal hypoxic-ischemic brain injury (induced by unilateral carotid artery ligation and 30 minutes at 8% oxygen in CD1 mice at postnatal day 9). Analyses are perfomed in the cerebellum, striatum/thalamus, and whole cortex. Examination of regional small RNA expression between four postnatal day 9 mouse pups after hypoxic-ischemic brain injury versus four sham surgery controls
2021-10-01 | GSE184995 | GEO
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:<p>Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.</p><p><br></p><p><strong>Untargeted fecal metabolomics</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4932' rel='noopener noreferrer' target='_blank'><strong>MTBLS4932</strong></a>.</p><p><strong>Targeted SCFA brain metabolomics</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4933' rel='noopener noreferrer' target='_blank'><strong>MTBLS4933</strong></a>.</p>
2022-10-12 | MTBLS4932 | MetaboLights
Project description:<p>Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.</p><p><br></p><p><strong>Targeted SCFA brain metabolomics</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4933' rel='noopener noreferrer' target='_blank'><strong>MTBLS4933</strong></a>.</p><p><strong>Untargeted fecal metabolomics</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4932' rel='noopener noreferrer' target='_blank'><strong>MTBLS4932</strong></a>.</p>
2022-10-12 | MTBLS4933 | MetaboLights
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 | GSE274183 | GEO