Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26435174_1.fastq.gz | Fastqsanger.gz | |||
| SRR26435174_2.fastq.gz | Fastqsanger.gz | |||
| SRR26435175_1.fastq.gz | Fastqsanger.gz | |||
| SRR26435175_2.fastq.gz | Fastqsanger.gz | |||
| SRR26435176_1.fastq.gz | Fastqsanger.gz |
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Project description:Edaravone dexborneol (EDB) is widely recognized for its anti-inflammatory and antioxidant properties and is clinically applied in the treatment of acute cerebral infarction. Ferroptosis is a critical process in the pathophysiology of brain injury following intracerebral hemorrhage (ICH). However, it remains unclear whether EDB can ameliorate ICH through the modulation of ferroptosis. This study aimed to evaluate the function and mechanism of EDB in treatment of ICH. With a rat ICH model, animal behavior tests, histopathological staining, magnetic resonance imaging and evans blue staining were used to evaluate the neural protective function of EDB on ICH rats. The potential molecular mechanism was investigated using RNA sequencing. With the administration of Fer-1, a range of ferroptosis-related biomarkers, including Fe2+, 4-hydroxynonenal, malondialdehyde, etc., were analyzed to to ascertain whether EDB confers neuroprotective effects through the modulation of P53/GPX4 pathways to inhibit ferroptosis. Finally, the findings were further corroborated using an in vitro ICH model with a P53 inhibitor. EDB has the potential to markedly enhance nerve and motor function, mitigate pathological damage, facilitate hematoma clearance, and repair BBB injury in ICH rats. KEGG analysis revealed that the differentially expressed genes were associated with signaling pathways, including P53 and ferroptosis. Both EDB and Fer-1 substantially reduced the concentrations of Fe2+, 4-hydroxynonenal, malondialdehyde, increased the amount of anti-oxidants, decreased the expression of P53, and concurrently upregulated the expression of GPX4. Besides, the P53 inhibitor PFT-α was observed to significantly reduce the levels of 4-HNE and lipid peroxides, while concurrently increasing the expression of GPX4. This investigation has shed light on the crucial neuroprotective role of EDB by regulating ferroptosis in ICH disease, which provided a theoretical basis for the clinical application of EDB in the treatment of ICH.
2025-01-27 | GSE288102 | GEO
Project description:Protein posttranslational modifications (PTMs) has been shown to regulate biological processes of human diseases via expanding the genetic code and for regulating cellular pathophysiology, however, the system-wide changes at the PTMs levels in ICH brain remains little known. Given that succinylation is one of the important PTMs in regulating many biological processes. Therefore, in this study, we used a high-resolution mass spectrometry-based, quantitative succinyllysine proteomics approach to firstly investigated the ICH-associated brain protein succinyllysine modifications. We totally identified the concentration of approximately 6000 succinylation events and quantified approximately 3500 sites. Among them, 25 succinyllysine sites on 23 proteins were increased, while 13 succinyllysine sites on 12 proteins were downregulated after ICH. Additionally, the subcellular localization analysis of these significantly changed succinylproteins showed that 58.3% hyposuccinylated proteins were located in the mitochondria, while the percentage of succinylproteins located in mitochondria was decreased to about 35% in ICH brains with concomitant increasing in the percentage of cytoplasm to 30.4%. Further bioinformatic analysis showed that the succinylated proteins were mostly located in mitochondria and synapse-related subcellular spaces, and participate in many pathophysiological processes, such as metabolism, cytoskeleton organization, synapse working and ferroptosis, etc.. Moreover, we performed a combination analysis of our succinylproteomics data with previously published transcriptome data and found that most of the differentially succinylated proteins were distributed into neurons, endothelial cells and astrocytes. In conclusion, our analyses uncover a number of succinylation-affected processes and pathways in ICH brains and provide new insights for understanding ICH pathophysiological processes.
2021-10-29 | PXD025621 | Pride
Project description:Ferroptotic cell death is dependent on unrestricted lipid peroxidation rather than activation of apoptotic effector caspases. A large number of ferroptosis activators have been reported recently. We used gene sequencing to analyze the effects of four ferroptosis activators (RSL3, N6F11, Fin56 and Erastin) on global gene expression in human PDAC1 cell line.
2023-10-18 | E-MTAB-12241 | biostudies-arrayexpress
Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor NRF2, we performed bulk RNA sequencing of perihaematomal and anatomically matched contralateral brain homogenate obtained at autopsy from a cohort of patients who died either within 24h of ICH or between 4-14 days of ICH onset, to investigate the spatiotemporal evolution of this Nrf2 activation.
2024-08-13 | E-MTAB-14323 | biostudies-arrayexpress
Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor Nrf2, particularly in mononuclear myeloid cells (for example, monocyte-derived cells (MdC) and microglia), we sought to determine the importance of Nrf2 to mononuclear myeloid cell responses and their impact on ICH pathology. We used intrastriatal injection of collagenase to induce ICH in both wild-type mice, and knockout mice with Cx3cr1-Cre-mediated excision of Nrf2 (Nfe2l2) exon 5.
2024-08-13 | E-MTAB-14324 | biostudies-arrayexpress
Project description:Introduction: Intracerebral hemorrhage (ICH) is a severe neurological disorder with no proven treatment. microRNA (miRNA) are short, noncoding nucleic acids that are critical regulators gene expression and promising novel therapeutic targets. Our prior research of mRNA-seq in swine demonstrated that ICH increased inflammatory gene expression within six hours of onset. We now present findings from an integrated analysis of miRNA-seq and mRNA-seq in peripheral blood mononuclear cells (PBMCs) from swine ICH. We tested the hypothesis that ICH would induce miRNA within six hours and that differentially expressed (DE) inflammatory genes would be targets of the DE miRNA. Methods: In 10 pigs, one PBMC sample was collected immediately prior to ICH induction and a second six hours later; miRNA-seq and mRNA-seq were performed. To determine the miRNA that primarily regulated the DE mRNA, an aggregate score was calculated for each miRNA of interest that incorporated the combined summary statistics of its DE target mRNA. Networks of molecular interactions were generated for the target mRNA and the combined miRNA/target mRNA. Results: A total of 227 miRNA were identified with alignment to the Sus scrofa (swine) genome, and 46 were DE (FDR <0.05). When analyzed with the aggregate scoring calculation, the miRNA that were most essential for regulating the DE mRNA included the following, all of which were downregulated post-ICH: miR-29a, miR-29b, miR-31, miR-34c, miR-125a, miR-132, miR-142, miR-150, miR-151a, miR-181a, and miR-186. A highly connected network of interactions was generated from these miRNA and their target mRNA. Conclusion: ICH strongly induced numerous miRNA/mRNA targets in swine PBMCs within six hours of onset. To our knowledge, this is the first integrated analysis of miRNA-seq and mRNA-seq in any study of ICH and the first report of miRNA in swine ICH. Further research is needed to determine whether these miRNA are potential therapeutic targets, including analyzing interventions such as miRNA overexpression or inhibition
2020-12-31 | GSE155242 | GEO
Project description:Disability or death secondary to intracerebral hemorrhage (ICH) is attributed to blood lysis, liberation of iron and generation of oxidative stress. Iron chelators bind free iron and prevent neuronal death induced by oxidative stress and disability due to ICH, but the mechanisms remain unclear. Here we show that the hypoxia-inducible factor prolylhydroxylase (HIF PHD) family of iron-dependent oxygen sensors is an effector of iron chelation in abrogating ICH-induced death. Molecular reduction of the three HIF PHD isoforms in mouse striatum improves functional recovery following ICH. A low molecular weight, hydroxyquinoline inhibitor of the HIF PHDs, which we call adaptaquin, reduces neuronal death and behavioral deficits following ICH in distinct rodent models. Unexpectedly, adaptaquin protects from oxidative death by suppressing ATF4- dependent prodeath gene expression rather than by activating a HIF-dependent prosurvival pathway. Adaptaquin treated neurons
2016-03-01 | E-GEOD-75048 | biostudies-arrayexpress
Project description:The protozoan Ichthyophthirius multifiliis (Ich) is a eukaryotic ciliate parasite of freshwater fish. Ich causes ichthyophthiriosis or ‘white spot disease’ characterized by white cysts covering the host skin and gills. The parasite is responsible for high mortalities and severe economic losses to farmed species as well as to ornamental species of fish. Despite the global importance of Ich, little is known about the genetic processes underlying its development and infectivity. Ich has three main life-stages, an infective theront, a parasitic trophont, and a reproductive tomont. To compare gene expression among Ich life-stages, oligonucleotide microarrays were constructed and utilized. All publicly-available Ich ESTs (~35K) were clustered to generate 9,129 unique consensus sequences represented as probes on custom microarrays produced in coordination with Roche NimbleGen. To facilitate comparative genomic analysis and to potentially increase gene content through cross-hybridization, gene coding sequences of related protozoans Tetrahymena thermophila and Plasmodium falciparum were also added to the microarrays. Gene expression was analyzed in samples taken from each of the three Ich life-stages. The results of this study will add in the understanding of protozoan global gene regulation and biology and should aid in the development of strategies aimed at the control of this important fish parasite. Submitted is a nine chip oligo array design using 385 K Nimblegen arrays. A total of nine microarrays were used for the experiment: three replicates from each of the three Ich life-stages (tomont, trophont, and theront life-stages). Probes were designed using 9,129 unique Ich ESTs (clustered contigs and singletons) as well as 26,273 Tetrahymena thermophila and 5,184 Plasmodium falciparum coding sequences. The probe design strategy was to create 12 60-mer oligonucleotide probes per I. multifiliis sequence, and 10 60-mer oligonucleotide probes for both T. thermophila and P. falciparum sequences. Total RNA was isolated in triplicate from the three life-stages of I. multifiliis and submitted to Nimblegen for labeling, hybridization, and scaning.
2011-09-30 | E-GEOD-18556 | biostudies-arrayexpress
Project description:We tested the hypothesis that circulating microRNAs (miRNAs) present in plasma might display a specific signature in patients with intracerebral hemorrhage (ICH). Global miRNA profiles were determined with the Agilent Human miRNA Microarray platform, 027233. ICH patients display a characteristic inflammation-related miRNA profile as compared to healthy controls.
2013-01-19 | GSE43618 | GEO
Project description:To identify the potential lncRNA and mRNA asscociated with Buyang Huanwu decoction (BYHWD) in treating intracerebral hemorrhage (ICH), we have employed lncRNA microarray expression profiling. 1596 and 1114 mRNAs were identified in the ICH vs sham group and the BYHWD vs ICH group, respectively. Specifically, 180 DEmRNAs were intersected among the three groups. 2287 and 2245 lncRNAs were identified in the ICH vs sham group and the BYHWD vs ICH group, respectively. Specifically, 342 DElncRNAs were intersected among the three groups. Expression of four mRNA (Spata2, Nkiras, Mef2c, Sh2b3) and lncRNA (Gm16045, Gm14005, Gm41118, 493304012Rik) from this signature was quantified by qPCR.
2023-07-01 | GSE220886 | GEO