Expression Profiles of Long Noncoding RNAs and mRNAs in Post-Cardiac Arrest Rat Brains
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ABSTRACT: To investigate lncRNA and mRNA expression profiles in post-cardiac arrest (CA) brains, an external transthoracic electrical current was applied for eight minutes to induce CA (the CA group). Four rats received sham-operations and served as the blank control (BC) group. Upon return of spontaneous circulation (ROSC), lncRNA and mRNA expression in the rat cerebral cortex was assayed with high-throughput Agilent lncRNA and mRNA microarrays. Thirty-seven lncRNAs were upregulated and 21 lncRNAs were downregulated in the CA group, and 258 mRNA transcripts were differentially expressed with 177 mRNAs upregulated and 81 mRNAs downregulated in the CA group.
Project description:Objective: To explore the mechanism of Jiangtang Tiaozhi Recipe in the treatment of obese T2DM patients with dyslipidemia based on transcriptomics. Methods: We chose 6 patients with obese type 2 diabetes mellitus and dyslipidemia (syndrome of excess of gastrointestinal heat) who were treated by JTTZR for 24 weeks, while 6 cases included in the healthy control group. We selected 6 cases in each group (disease group before treatment, disease group after treatment and healthy control group) to start the research of lncRNA microarray. According to the differentially expressions of lncRNAs and mRNAs, we secondly performed GO analysis, Pathway analysis, and found out some target lncRNAs as well as their associated mRNAs. The trial register number is NCT04623567. Results: (1) Disease group before treatment vs. healthy control group: There are 557 upregulated lncRNAs, 273 downregulated lncRNAs, 491 upregulated mRNAs and 1639 downregulated mRNAs. (2) Disease group after treatment vs. Disease group before treatment: There are 128 upregulated lncRNAs, 32 downregulated lncRNAs, 45 upregulated mRNAs and 140 downregulated mRNAs.
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.
Project description:We identified 177 lncRNAs and 153 mRNAs that were differentially expressed (â?¥ 2-fold change), indicating that many lncRNAs are significantly upregulated or downregulated in AF. Among these, NONHSAT040387 and NONHSAT098586 were the most up-regulated and downregulated lncRNAs, and were selected for validation via quantitative PCR. GO analysis and KEGG pathway were applied to exploring potential lncRNAs function, identifying several pathways were alerted in atrial fibrillation pathogenesis. we investigated the expression patterns of lncRNAs and mRNAs from atrial fibrillation with Agilent Human lncRNA array V4.0 (4 Ã? 180 K), which include 78,243 human lncRNAs and 30,215 coding transcripts.
Project description:Long non-coding RNAs (lncRNAs) are involved in cancer progression. In this study, the lncRNA profiling were analyzed in chemoresistant and sensitive breast cancer cells. We found a group of dysregulated lncRNAs in chemoresistant cells. Expression of dysregulated lncRNAs are correlated with dysregulated mRNAs, and enriched in GO and KEGG pathways related with cancer progression and chemoresistance development. Within those lncRNA-mRNA interactions, some lncRNAs may cis-regulate neighboring protein coding genes and involved in chemoresistance. The lncRNA NONHSAT028712 was then validated to regulate nearby CDK2 and interfere with cell cycle and chemoresistance. Furthermore, we identified another group of lncRNAs trans-regulated gene expression via interacting with different transcription factors (TF). Whereby NONHSAT057282 and NONHSAG023333 was found to modulate chemoresistance and most likely interacted with ELF1 and E2F1 respectively. In conclusion, this study reported for the first time the lncRNA expression patterns in chemoresistant breast cancer cells, and provided a group of novel lncRNA targets in mediating chemoresistance development in both cis- and trans- action mode. MCF-7/ADM replication 3 times, MCF-7/WT replication 3 times
Project description:In this study,compared with normal group, there were 94 differentially expressed lncRNAs and 83 mRNA transcripts in TOF (P<0.05). Correlation analysis between lncRNA and mRNA further showed that differentially expressed lncRNA can be linked to mRNAs, suggesting the regulator role of lncRNA in mRNA expression
Project description:Chlamydia trachomatis (C. trachomatis) is a major etiological agent of sexually transmitted infection. Some stressing conditions can result in persistent chlamydial infection, which is thought to associate with severe complications such as ectopic pregnancy and tubal factor infertility. Long noncoding RNAs (lncRNAs) have been identified as key modulators in many biological processes. However, the role of lncRNAs in persistent chlamydial infection is still unclear. In this study, we used lncRNA and mRNA microarray to identify the global lncRNAs and mRNAs expression in penicillin-induced persistent chlamydial infection in HeLa cells as well as the control group (HeLa cells without C. trachomatis infection). Among 1005 differentially expressed lncRNAs, 585 lncRNAs were upregulated and 420 downregulated in persistent chlamydial infection, while 410 mRNAs were identified to express differentially, of which 113 mRNAs were upregulated and 297 downregulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis with differentially expressed genes were performed. We then constructed the lncRNA-miRNA-mRNA competing endogenous RNAs (ceRNAs) network. Four mRNAs were validated to be changed by quantitative real-time PCR which were correlated with the microarray result. Integration of protein-protein interaction (PPI) network was constructed and hub genes were identified. These findings provide a new perspective on the molecular mechanism of penicillin-induced persistent chlamydial infection.
Project description:Our present study analyzes decidual natural killer(dNK) cells expression profiles of the lncRNA and mRNA in missed abortional patients. A total of 276 mRNAs and 67 lncRNAs were identified to be significantly dysregulated in missed abortion (p<0.01). Subsequently, the potential function of dysregulated mRNAs and lncRNAs in missed abortion were explored through the bioinformatics method. In addition, the relationship between these dysregulated lncRNAs and mRNAs was revealed through constructing the lncRNA-mRNA interaction network. Our data showed that upregulated mRNAs were enriched in immune response and cytokine-cytokine receptor interaction while downregulated mRNAs were mainly related to cell adhesion and ECM-receptor interaction. Most importantly, several novel lncRNAs in dNKs, regulating core maternal-fetal interface activation-related mRNAs, were algorithmically predicted, indicating involvement of lncRNAs in the pathogenesis in early missed abortion.Topology analysis of lncRNA-mRNA interaction network suggested that the network presented a small world property, which means that most of mRNAs in the network were regulated by relative small number of hub lncRNAs. This study paves the way of investigating pathogenesis of early human missed abortion and facilitating the development of novel missed abortion therapeutics targeting lncRNAs.
Project description:To identify the potential lncRNA and mRNA post intracerebral hemorrhage (ICH), we have employed lncRNA microarray expression profiling. 570 mRNAs and 313 lncRNAs were identified in the ICH vs sham group .Expression of six mRNA (Saa3, Col10a1, Mmp13, Oxt, Pcdhb6 and Resp18) and lncRNA (ENSMUT00000141700, AK143011, ENSMUT00000128306, AK030988, ENSMUST00000187076 and ENSMUST00000134129) from this signature was quantified by qPCR.
Project description:Abstract: Backgroud: This study was to explore long noncoding RNA (lncRNA) and messenger RNA (mRNA) expression profiles and construct functional networks to analyze their biological functions when botulinum toxin type A (BTXA) inhibited salivary secretion. Methods: BTXA and saline were injected into the submandibular gland of rats as the BTXA group and control group, respectively. Morphological and secretory function tests validated the animal models. Microarray analysis was applied to identify the expression variation of lncRNA and mRNA and were confirmed by qRT-PCR. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to explicit the biological functions. The construction of functional networks including lncRNA-mRNA co-expression network and competing endogenous RNA (ceRNA) network was to reveal the interaction between coding and noncoding genes. Results: A total of 254 lncRNAs and 631 mRNAs were differentially expressed (DE) between the control group and the BTXA group. Ten lncRNAs and eleven mRNAs were confirmed by qRT-PCR and the results were consistent with the microarray analysis. The bioinformatic analysis found that most of mRNAs were closely related to transmembrane transporter activity. LncRNA-mRNA co-expression network and ceRNA network were constructed and identified several critical mRNA-lncRNA axes and key microRNAs related to salivary secretion, respectively. Conclusions: Our study identified DE lncRNAs and mRNAs through microarray analysis and explored the biological functions and interaction between coding and noncoding genes through bioinformatics analysis. These findings may provide new directions for the mechanism of BTXA to inhibit salivary secretion.
Project description:Spinal cord injury (SCI) is a severely disastrous event that occurs in the central nervous system (CNS) that is associated with high disability and mortality rates.To further explore the expression of mRNAs and lncRNAs and the potential roles of differentially expressed mRNAs and lncRNAs after SCI, we examined the expression of mRNAs and lncRNAs in a rat model at 2 hours, 2 days and 7 days after SCI and identified the differentially expressed lncRNAs (DE lncRNAs) and differentially expressed mRNAs (DE mRNAs) using microarray analysis. A total of 992 mRNAs were differentially expressed at 2 hours after SCI, among which 730 mRNAs were up-regulated and 262 mRNAs were down-regulated. A total of 4308 mRNAs were differentially expressed at 2 days after SCI, including 2229 mRNA with up-regulated expression and 2079 mRNAs with down-regulated expression. A total of 4113 mRNAs were differentially expressed at 7 days after SCI, including 2339 up-regulated and 1774 down-regulated mRNAs. After SCI, 772 lncRNAs were differentially expressed in the 2-hour group (528 were up-regulated, 244 were downregulated) , 3193 lncRNAs were differentially expressed in the 2-day group (1332 were up-regulated, 1861 were downregulated) ,3093 lncRNAs were differentially expressed in the 7-day group (1290 were up-regulated, 1803 were downregulated) .The current study on provides novel insights into how lncRNAs and mRNAs regulate the pathogenesis of the immediate phase after SCI.