Altered expression profile of long non-coding RNA and mRNA in mice cortex around injury focus after traumatic brain injury
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE79441 | GEO | 2018/04/13
REPOSITORIES: GEO
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Project description:We report the altered expression profiles of lncRNA and mRNA in mice cortex after subarachnoid hemorrhage (SAH). Total of 615 lncRNAs transcripts and 441 mRNAs transcripts were aberrantly expressed at 24 hours after SAH. SAH was induced in C57BL/6 mcie. The LncRNA and mRNA expression profiles in cortex of normal mice and SAH mice were examined by RNA-Seq.
2016-03-22 | E-GEOD-79416 | biostudies-arrayexpress
Project description:We report the altered expression profiles of lncRNA and mRNA in mice cortex after subarachnoid hemorrhage (SAH). Total of 617 lncRNAs transcripts and 444 mRNAs transcripts were aberrantly expressed at 24 hours after SAH.
2016-03-22 | GSE79416 | GEO
Project description:It is commonly observed that patients with bone fracture concomitated with traumatic brain injury (TBI) had significantly increased fracture healing while the underlying mechanisms were not fully revealed. Long non-coding RNAs (lncRNAs) were known for paly complicated roles in bone homeostasis while its role in TBI accelerated fracture were rarely reported. The present study was designed to determine the role of lncRNAs in TBI accelerated fracture via transcriptome sequencing and further bioinformatical analysis. Blood samples from 3 fracture only patients, 3 fracture concomitated with TIB patients and 3 healthy controls were harvested and were subsequently subjected to transcriptome lncRNAs sequencing. Differentially expression genes were identified, and pathway enrichment were performed by Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyze. High high-dimensional data portraying by self-organizing map (SOM) machine learning was applied to further interpret the data. A xCell method were then used to predict cellular behavior in all samples based on gene expression profiles and a lncRNA-cell interaction network were generated. A total of 874 differentially expressed genes were identified, of which about 26% were lncRNAs. Those identified lncRNAs were mainly enriched on traumatic brain injury related- and damage repair related-pathways. SOM analyzes revealed that those differentially expressed lncRNAs could be divided into three major module implications and were mainly enriched on transcriptional regulation and immune related signal pathways, which promote us to further explore cellular behaviors based on differentially expressed lncRNAs. We have predicted that basophils, CD8+ T effector memory cells, B cells, and naïve B cells were significantly down-regulated while microvascular endothelia cells were predicated significantly up-regulated with TBI/Fr group was the lowest or highest, respectively. ENSG00000278905, ENSG00000240980, ENSG00000255670, and ENSG00000196634 were the most differentially expression lcnRNA that related to all changes of cellular behavior. The present study has revealed for the first time that several critical lncRNAs may participate in TBI accelerated fracture potentially via regulating cellular behaviors of basophils, cytotoxic T cells, B cells and endothelia cells.
2021-05-24 | GSE171718 | GEO
Project description:With the aim of exploring expression profiles and biological functions of long non-coding RNA (lncRNA) and mRNAs after ischemia-reperfusion injury (SCII), differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) in rat spinal cords were identified following SCII through high-throughput RNA sequencing. In total, 1455 lncRNAs and 6707 mRNAs were observed to be differentially expressed (FC ≥1.5 and P <0.05) after SCII, including 761 up-regulated and 694 down-regulated lncRNAs and, 3772 up-regulated and 2935 down-regulated mRNAs.
2019-12-08 | GSE138966 | GEO
Project description:Evidence supports the contribution of long non-coding RNAs (lncRNAs) and ferroptosis to traumatic brain injury (TBI) pathogenesis. However, lncRNA regulation in TBI-induced ferroptosis remains poorly understood. Herein, we identified an lncRNA, named noncoding transcript of chemokine (C-C motif) ligand 4 (Ccl4) overlapping (Ntoco), which was upregulated in TBI mice. The upregulation was initiated by hypoxia ischemia induced lower enrichment of H3K27me3 on the Ntoco promoter. Ntoco knockdown inhibited neuron ferroptosis, ameliorated spatial memory and lesion volume following TBI. Ntoco overexpression promoted neuron ferroptosis and recruited microglia to provoke an inflammatory response via Ccl4. Mechanistically, Ntoco facilitated K48-linked ubiquitination and protein degradation by binding to Hnrnpab, which suppressed NF-κB/Lcn2 signal axis activation, including decreased phosphorylation of IkBα, increased phosphorylation of IKKα/β, nuclear translocation of the NF-κB p65 subunit, and elevated Lcn2 expression. These data indicated that targeting Ntoco to mitigate ferroptosis might be a potential therapeutic strategy for TBI.
2024-06-21 | GSE235523 | GEO
Project description:Chemoresistance is a major cause of poor prognosis of breast cancer.More and more mRNAs and lncRNAs are reported to upregulate chemoresistance in breast cancer.To explore the how mRNAs and lncRNAs involved in chemoresistance of breast cancer,we sceened upregulated mRNAs and lncRNA from parental MCF-7 , chemoresistant MCF-7 cells as well as 4 breast cancer tissue sensitive to chemotherapy and 4 resistant to chemotherapy . Total RNA was extracted using Trizol reagent. Agilent Human lncRNA Microarray V6 (4*180K) was used to analyze the global profiling of human lncRNAs and protein-coding transcripts in these samples. The microarray contains 83,835 lncRNAs and 27,233 coding genes.
2020-02-25 | E-MTAB-8787 | biostudies-arrayexpress
Project description:The identification of the expression patterns of long non‑coding RNAs (lncRNAs) and mRNAs in the kidney under normal and renal ischemia/reperfusion (IR) conditions is essential for understanding the genetic mechanisms underlying the pathogenesis of renal IR injury. Here, we have carried out a genome-wide long non-coding RNA and mRNA microarray analysis in mice kidneys with IR. The data revealed that the expression profiles of lncRNAs and mRNAs in the kidneys differed markedly between the Sham group and IR group, and in total 276 differentially expressed (>2‑fold) lncRNAs (201 upregulated, 75 downregulated) and 267 mRNAs (192 upregulated, 75 downregulated) were identified. qRT-PCR analysis was performed to verify the expression patterns of several lncRNAs and mRNAs.We found a specific and strongly differentially expressed lncRNA, an renal ischemia-reperfusion (IR) injury associated RNA, termed lncRNA-IRAR, which was mainly located in tubular epithelia cells. In vitro and in vivo gain- or loss-of-function studies were performed to investigate the role of lncRNA-IRAR during renal IRI. Moreover, an expression volcano map of the differentially expressed mRNAs showed that UCP1 was the most dramatically downregulated gene, and its role in oxidative stress and apoptosis was assessed both in vitro and in vivo. Genetic deletion of UCP1 was used to investigate the effects of UCP1 on ischemia -indued acute kidney injury in mice.
2019-05-21 | GSE131454 | GEO
Project description:Background: Long non-coding RNAs (lncRNAs) are increasingly implicated as gene regulators and may ultimately be more numerous than protein-coding genes in the human genome. Despite large numbers of reported lncRNAs, reference annotations are likely incomplete due to their lower and tighter tissue-specific expression compared to mRNAs. An unexplored factor potentially confounding lncRNA identification is inter-individual expression variability. Here, we characterize lncRNA natural expression variability in human primary granulocytes. Results: We annotate granulocyte lncRNAs and mRNAs in RNA-seq data from ten healthy individuals, identifying multiple lncRNAs absent from reference annotations, and use this to investigate three known features (higher tissue-specificity, lower expression, and reduced splicing efficiency) of lncRNAs relative to mRNAs. Expression variability was examined in seven individuals sampled three times at one or more than one month intervals. We show that lncRNAs display significantly more inter-individual expression variability compared to mRNAs. We confirm this finding in 2 independent human datasets by analyzing multiple tissues from the GTEx project and lymphoblastoid cell lines from the GEUVADIS project. Using the latter dataset we also show that including more human donors into the transcriptome annotation pipeline allows identification of an increasing number of lncRNAs, but minimally affects mRNA gene number. Conclusions: A comprehensive annotation of lncRNAs is known to require an approach that is sensitive to low and tight tissue-specific expression. Here we show that increased inter-individual expression variability is an additional general lncRNA feature to consider when creating a comprehensive annotation of human lncRNAs or proposing their use as prognostic or disease markers. We used PolyA+ RNA-seq data from human primary granulocytes of 10 healthy individuals to de novo annotate lncRNAs and mRNAs in this cell type and ribosomal depleted (total) RNA-seq data from seven of these individuals sampled three times to analyze lncRNA amd mRNA expression variability
2016-01-05 | E-GEOD-70390 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs) are important regulators of cell fate, and their mis-expression has been implicated in many diseases. While distinct polymerases generate messenger vs. noncoding ribosomal or tRNAs3, little is known about distinct mechanisms controlling lncRNA expression. Here we show that transcription of lncRNAs is quantitatively different from that of messenger RNAs (mRNAs)--as revealed by deficiency of Dicer (Dcr), a key ribonuclease that generates microRNAs (miRNAs). Loss of Dcr in mouse embryonic stem cells (mESCs) led surprisingly to decreased level of the majority of lncRNAs. The canonical Dgcr8-Dcr-miRNA pathway is required for robust lncRNA expression, at the level of transcriptional initiation and elongation of lncRNA genes rather than at the level of their stability. cMyc, an oncogenic transcription factor, whose expression is indirectly regulated by Dcr-miRNA in mESCs, is partly responsible for lncRNA transcription. Loss of cMyc led to a more dramatic decrease of lncRNAs than mRNAs, and cMyc overexpression rescues lncRNA expression in Dcr KO cells. A quantitative metric of “mRNA-lncRNA decoupling” revealed that Dcr and cMyc differentially regulate lncRNAs vs. mRNAs in diverse cell types and in vivo, as evidenced by hundreds of microarray experiments. Thus, Dcr and cMyc may allow numerous lncRNAs to be activated or deactivated as a class, implicating lncRNAs to potential regulatory roles in development and disease states where Dcr and cMyc have been associated with. RNA was sequenced from WT and Dcr KO mESCs and the expression of lncRNAs and mRNAs are compared between WT and Dcr KO mESCs.
2014-06-15 | E-GEOD-55338 | biostudies-arrayexpress
Project description:Spinal cord injury (SCI) is a serious disorder of the central nervous system with a high disability rate. Long non-coding RNAs (lncRNAs) are reported to mediate many biological processes. The aim of this study was to explore lncRNA and mRNA expression profiles and functional networks after SCI.We identified 5465 differentially expressed lncRNAs (DE lncRNAs) and 8366 differentially expressed mRNAs (DE mRNAs) in the SCI group compared with the sham group (fold change >2.0, P<0.05). Four genes were confirmed by real-time PCR which were consistent with the microarray data. GSEA analysis showed that most marked changes occurred in pathways related to immune inflammation and nerve cell function, including cytokine-cytokine receptor interaction (rno04060), TNF signaling pathway (rno04668), neuroactive ligand-receptor interaction (rno04080)，and GABAergic synapse (rno04727). Enrichment analysis identified 30 signaling pathways, including those associated with inflammation and the immune response. A total of 40 key lncRNAs were identified using the SVM-RFE algorithm. A key lncRNA-mRNAs co-expression network was generated for 230 951 lncRNA-mRNA pairs with half showing positive correlations. Several key DE lncRNAs were predicted to have “cis” or “trans”-regulated target genes. The transcription factors, Sp1, JUN, and SOX10, may regulate the interaction between XR_001837123.1 and ETS 1. In addition, five pairs of ceRNA regulatory sequences were identified.
2023-01-01 | GSE218088 | GEO