TableNONMMUT140591.1 may serve as a ceRNA to regulate Gata5 in UT-B knockout-induced cardiac conduction block
Ontology highlight
ABSTRACT: Objective: We intended to explore the potential molecular mechanisms underlying cardiac conduction block inducted by UT-B deletion at the transcriptome level. Methods: The heart tissues were harvested from UT-B null mice and age-matched wild-type mice for lncRNA sequencing analysis. Based on the sequencing data, the differentially expressed mRNAs (DEMs) and lncRNAs (DELs) between UT-B knockout and control groups were identified, followed by function analysis and mRNA-lncRNA co-expression analysis. The miRNAs were predicted, and then the competing endogenous RNA (ceRNA) network was constructed. Results: UT-B deletion results in the aberrant expression of 588 lncRNAs and 194 mRNAs. These DEMs were significantly enriched in inflammation-related pathway. A lncRNA-mRNA co-expression network and a ceRNA network was constructed on the basis of the DEMs and DELs. C7 (complement C7)-NONMMUT137216.1 co-expression pair had the highest correlation coefficient in the co-expression network. NONMMUT140591.1 had the highest degree in ceRNA network and involved in ceRNA of NONMMUT140591.1-mmu-miR-298-5p-Gata5 (GATA binding protein 5). Conclusion: UT-B deletion may promote cardiac conduction block via inflammatory process. The ceRNA NONMMUT140591.1-mmu-miR-298-5p-Gata5 may be a potential molecular mechanism of UT-B knockout-induced cardiac conduction block.
Project description:Aim To identify transcript level differences between healthy and osteoarthritis meniscus in human keen joint using RNA-seq.Methods human menisci were isolated from non-OA patients and OA patients during arthroscopic surgery (N=5). Based on the RNA sequencing, differentially expressed lncRNAs (DELs) and mRNAs (DEMs) were screened.Expression level of selected autophagy-related lncRNAs and mRNAs was validated by real-time qPCR.Results we identified 310 DELs and 320 DEMs, and found five upregulated and one downregulated autophagy-related DEMs. After reverse prediction of miRNA, paired miRNA–lncRNA interactions and verification by RT-qPCR, the ceRNA regulatory networks were constructed consisting of two lncRNAs (PCAT19, CLIP1-ASA) and two mRNAs (BAG3 and HSP90AB1). Finally, GSEA indicated that the increased expressions of autophagy-related mRNAs inhibited the glycosaminoglycan biosynthesis in the degenerative meniscus.Conclusions for the first time ,we constructed an autophagy-related lncRNA-miRNA-mRNA regulatory ceRNA network based on RNA sequencing and experimental validation, which might provide new mechanistic insights and potential therapeutic targets for meniscal degeneration.
Project description:Tibetan chicken has a suite of adaptive features to tolerate the high-altitude hypoxic environment as a unique native breed in Qinghai-Tibet Plateau of China. Increasing evidence suggests that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have roles in hypoxic adaptation of high-altitude animals, though their exact contributions remain unclear. This study aims to uncover the global landscape of mRNAs, lncRNAs and miRNAs using transcriptome sequencing so as to construct a regulatory network of competing endogenous RNAs (ceRNAs) provide a new sight for the hypoxic adaptation of Tibetan chicken embryos. In the study, 354 differentially expressed mRNAs (DEGs), 389 differentially expressed lncRNAs (DELs) and 73 differentially expressed miRNAs (DEMs) were identified between Tibetan (TC) and Chahua chicken (CH). The functional analysis showed that several important DEMs and their targets of DELs and DEMs are involved in angiogenesis (include blood vessel development and blood circulation) and energy metabolism (include glucose, carbohydrate and lipid metabolism). The ceRNA network was then constructed with the predicted pairs of DEGs-DEMs-DELs which further revealed regulatory roles of these differentially expressed RNAs in hypoxic adaptation of Tibetan chicken.
Project description:we conducted transcriptome and small RNA sequencing to identify differentially expressed genes (DEGs), miRNAs (DEMs), and lncRNAs (DELs). Function analysis on DEM-target genes can explain the regulatory roles of miRNAs in LC. The lncRNA-miRNA pairs, miRNA-mRNA pairs, and lncRNA-mRNA pairs were identified, which were then combined to construct the interplay of lncRNAs/miRNAs/mRNAs. And we used the online databases to verify the selected DEMs, DELs, and DEGs. Our study identified 2509 DEGs, 34 DEMs, and 432 DELs in LC patients. miRNA-mRNA pairs, including 1 miRNA (hsa-miR-21-5p) and 5 targeted genes (RECK, TIMP3, EHD1, RASGRP1 and ERG), were figured out. We finally found the hub subnetwork (LINC00632/has-miR-21-5p/TIMP3) by combining lncRNA-miRNA pairs, miRNA-mRNA pairs and lncRNA-mRNA pairs.
Project description:We conducted transcriptome and small RNA sequencing to identify differentially expressed genes (DEGs), miRNAs (DEMs), and lncRNAs (DELs). Function analysis on DEM-target genes can explain the regulatory roles of miRNAs in LC. The lncRNA-miRNA pairs, miRNA-mRNA pairs, and lncRNA-mRNA pairs were identified, which were then combined to construct the interplay of lncRNAs/miRNAs/mRNAs. And we used the online databases to verify the selected DEMs, DELs, and DEGs. Our study identified 2509 DEGs, 34 DEMs, and 432 DELs in LC patients. miRNA-mRNA pairs, including 1 miRNA (hsa-miR-21-5p) and 5 targeted genes (RECK, TIMP3, EHD1, RASGRP1 and ERG), were figured out. We finally found the hub subnetwork (LINC00632/has-miR-21-5p/TIMP3) by combining lncRNA-miRNA pairs, miRNA-mRNA pairs and lncRNA-mRNA pairs.
Project description:Echinococcus multilocularis (Em) infection and the growth and proliferation of its metacestode within the liver of hosts are related to complex host–parasite interactions at the molecular level. However, the profiles of long non-coding RNAs (lncRNAs) and mRNAs of mice in response to Em are poorly understood. In this study, we detected numerous differentially expressed lncRNAs (DELs) and mRNAs (DEMs) in the mouse liver at eight time points after Em infection. Some DEMs and DELs were found continuously dysregulated. These DEMs were notably enriched in the “antigen processing and presentation,” “Th1 and Th2 cell differentiation” and “Th17 cell differentiation” pathways.
Project description:In this research, 90 differential expression mRNAs (DEMs), 72 differential expression lncRNAs (DELs) and biological functions and pathway were identified in ulcerative colitisby (UC) integrated analysis. Potential therapeutic target for treatment was preliminary verified by qRT-PCR experiment and bioinformatics analysis.
Project description:Gata factors are amongst the genes expressed early on in the process of cardiogenesis. We used microarrays to examine the immediate early targets of Gata4 and Gata5 in the Xenopus leavis animal cap cardiogenesis model. We hope to use these data to examine the roles of Gata4 and Gata5 in cardiogenesis and also to begin to dissect out the common and distinct targets of Gata4 and Gata5. Experiment Overall Design: Xenopus leavis embryos were injected at the one cell stage with dexamethasone-inducible Gata4 or Gata5 mRNA constructs (to examine endodermal and mesodermal targets) or with Gata4 in the presence of Dkk1 (to examine mesodermal targets.) Embryos were cultured to stage 9, whereupon animal caps were excised and cultured for 2.5 hours in media containing dexamethasone to induce the constructs and cycloheximide to block de novo protein synthesis and thus give only immediate early targets.
Project description:Arrhythmias are a hallmark of myocardial infarction (MI) and increase patient mortality. The cardiac conduction system is implicated in arrhythmias, but how it is altered following MI is poorly understood. We demonstrate complete conduction system restoration during neonatal mouse heart regeneration, versus pathological remodelling at non-regenerative stages. Tissue-cleared whole-organ imaging identified disorganised bundling of conduction fibres after MI, global His/Purkinje disruption and regional loss of connexin-40. Single-cell RNA-sequencing revealed that Purkinje cells undergo specific molecular changes to regenerate the network, versus sustained aberrant electrical alterations during fibrotic repair. This manifested functionally as transition from normal rhythm to pathological conduction delay beyond the regenerative window. Modelling the non-regenerative phenotype in the infarcted human heart implicated these changes as causative for bundle branch block and ventricular dyssynchrony, as observed in patients. These findings elucidate the mechanisms underpinning conduction system regeneration versus repair and reveal the consequences of MI-induced damage for clinical arrhythmogenesis.