Similar Datasets
Project description:Plasma ceRNA expression profiles were acquired by using a human ceRNA microarray.
2020-04-14 | GSE148602 | GEO
Project description:Circulating long noncoding RNAs associated with hypertrophic cardiomyopathy
| PRJNA601680 | ENA
Project description:Hypertrophic cardiomyopathy (HCM) is one of the most commonly inherited heart diseases and the leading cause of sudden cardiac death among adolescents and young adults. Circulating long noncoding RNAs (lncRNAs) have demonstrated potential as diagnostic and therapeutic targets in several cardiovascular diseases. However, the circulating extracellular lncRNA expression profile of patients with HCM remains unclear. Plasma lncRNA expression was evaluated in patients with HCM and healthy controls using a human lncRNA microarray. A weighted correlation network analysis (WGCNA) and linear models for microarray data (Limma) were used. GSE68316 data from cardiac tissue in the Gene Expression Omnibus database were analysed for further validation. Using WGCNA, two modules (referred to as the magenta and the light?yellow module) were identified that were positively associated with HCM. Gene Ontology analysis revealed that lncRNAs in the magenta module targeted 'heart growth'. Using Limma, a total of 290 lncRNAs were differentially expressed (210 upregulated and 80 downregulated) in the plasma of HCM patients, compared with controls. Moreover, combined WGCNA and Limma analysis demonstrated that 27 hub lncRNAs in the magenta module and 13 hub lncRNAs in the light?yellow module were significantly upregulated, compared with the controls. Moreover, of the 40 differentially expressed hub lncRNAs identified in the two modules, three circulating lncRNAs (lnc?P2RY6?1:1, ENST00000488040 and ENST00000588047) were also significantly upregulated in the HCM cardiac tissue validation dataset. These lncRNAs may serve as biomarkers and therapeutic targets for precise diagnosis and treatment of HCM.
| S-EPMC7646839 | biostudies-literature
Project description:Approximately 1426 lncRNAs (965 up-regulated and 461 down-regulated) and 1715 mRNAs (896 up-regulated and 819 down-regulated) were aberrantly expressed in HCM patients with fold change > 2.0 Myocardial tissues were obtained from 7 HCM patients and 5 disease-free individuals, and lncRNA and mRNA expression profiles were analyzed using the CapitalBio Human LncRNA Microarray v2.0.
2015-05-08 | E-GEOD-68316 | biostudies-arrayexpress
Project description:Hypertrophic cardiomyopathy (HCM) is the most common form of hereditary cardiomyopathy. It is characterized by an unexplained non-dilated hypertrophy of the left ventricle with a conserved or elevated ejection fraction. It is a genetically heterogeneous disease largely caused by variants of genes encoding for cardiac sarcomere proteins, including MYH7, MYBPC3, ACTC1, TPM1, MYL2, MYL3, TNNI3, and TNNT23. Preclinical evidence indicates that the enhanced calcium sensitivity of the myofilaments plays a key role in the pathophysiology of HCM. Notably, this is not always a direct consequence of sarcomeric variations but may also result from secondary mutation-driven alterations. Long non-coding RNAs (lncRNAs) are a large class of transcripts ≥200 nucleotides in length that do not encode proteins. Compared to coding mRNAs, most lncRNAs are not as well-annotated and their functions are greatly unexplored. Nevertheless, increasing evidence shows that lncRNAs are involved in a variety of biological processes and diseases including HCM. Accumulating evidence has indicated that lncRNAs are dysregulated in HCM, and closely related to sarcomere construction, calcium channeling and homeostasis of mitochondria. In this review, we have summarized the known regulatory and functional roles of lncRNAs in HCM.
| S-EPMC8430576 | biostudies-literature
Project description:Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiomyopath that caused by mutations in genes encoding proteins of the cardiac sarcomere. Although multiple efforts have been made to understand the pathogenesis of HCM, the mechanisms of how long noncoding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) network result in HCM still unkown. Herein, we acquired the different expression profiles of lncRNAs (DElncRNAs) and messenger RNAs (mRNA, DEGs) by using microarray, microRNAs (DEmiRNAs) by sequencing in plasma of HCM patients and healthy controls. LncRNA-miRNA pairs were predicted using miRcode and starBase, and crossed with DEmiRNAs. MiRNA-mRNA pairs were retrieved from miRanda and TargetScan, and crossed with DEGs. Combined these pairs, the ceRNA network was constructed and hub nodes were then analyzed to reconstruct subnetwork. Gene Ontology and KEGG pathways were used to analyse the mRNAs in the ceRNA. Total 520 DElncRNAs, 33 DEmiRNAs, and 371 DEGs were identified. By coexpression analysis, 682 lncRNA-mRNA pairs were identified with a coefficient ≥ 0.9 and p < 0.05. The ceRNA network with 8 lncRNAs, 3 miRNAs and 22 mRNAs was constructed visualized by Cytoscape. LncRNA RP11-66N24.4 and LINC00310 are among the top 10% nodes and the associated ceRNA subnetwork may be the center of the whole ceRNA network. Furthermore, the qRT-PCR results showed that LINC00310 was signifcantly decreased in HCM patients. For LINC00310, GO analysis revealed that the biological processes was enriched in cardiovascular system development, sprouting angiogenesis, circulatory system development and so on, and Pathway analysis was mainly enriched in cGMP-PKG signaling pathway. Our study reveals the novel lncRNA-related ceRNA network in HCM and the identified lncRNA LINC00310 may be roles in the pathogenesis mechanisms of HCM, which could provide further insight into the pathogenesis of HCM.
2022-09-28 | GSE197218 | GEO
Project description:Long non-coding RNAs (lncRNAs) are generally defined as RNA transcripts longer than 200 nucleotides that are not translated into proteins. Recently, many small open reading frames (smORFs) embedded in lncRNA scripts have been verified to be able to encode functional polypeptides (namely lncRNA-SEPs here). Although collaborative analysis by advanced genomics, bioinformatics and proteomics largely drives SEPs discovery, the poor predictability, diminutive size and low abundance still challenge systematic identification of SEPs from different biological samples. Here, we took advantage of the NONCODE database that deposited with the most complete collection and annotation of lncRNA transcripts from different species to build a database that to maximally collect all putative small ORFs from human and mouse lncRNA transcripts. Two effective and complementary polypeptides enrichment strategies (30 kDa MWCO filter and C8 SPE column) were also integrated to further improve the discovery of novel lncRNA-SEPs. These efforts led to the discovery of 362 lncRNA-SEPs from 8 human cell lines and 238 lncRNA-SEPs from 3 mouse cell lines and 8 mouse tissues. 18 out of these lncRNA-SEPs were verified experimentally by multiple technologies including in vitro expression, immunoblotting and parallel reaction monitoring-based mass spectrometry (PRM-MS) in 293T cells. Further bioinformatic analysis reveals that the physical and chemical properties of these novel lncRNA-SEPs, such as amino acid composition and codon usage, are varied from canonical proteins. Intriguingly, nearly 70% of the identified lncRNA-SEPs were found to be initiated with non-AUG start codons. Collectively, the efficient workflows presented in this study enables us identify 600 novel lncRNA-SPEs from multiple cell lines and tissues, which should represent the largest number of MS-detected lncRNA-encoding SEPs ever reported to date. These novel lncRNA-SEPs not only could provide new clues for the annotation of the noncoding elements in the genome, but also could serve as a valuable resource for the functional characterization of individual lncRNA-SEPs.
2023-05-06 | PXD016981 | Pride
Project description:Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiomyopath that caused by mutations in genes encoding proteins of the cardiac sarcomere. Although multiple efforts have been made to understand the pathogenesis of HCM, the mechanisms of how long noncoding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) network result in HCM still unkown. Herein, we acquired the different expression profiles of lncRNAs (DElncRNAs) and messenger RNAs (mRNA, DEGs) by using microarray, microRNAs (DEmiRNAs) by sequencing in plasma of HCM patients and healthy controls. LncRNA-miRNA pairs were predicted using miRcode and starBase, and crossed with DEmiRNAs. MiRNA-mRNA pairs were retrieved from miRanda and TargetScan, and crossed with DEGs. Combined these pairs, the ceRNA network was constructed and hub nodes were then analyzed to reconstruct subnetwork. Gene Ontology and KEGG pathways were used to analyse the mRNAs in the ceRNA. Total 520 DElncRNAs, 33 DEmiRNAs, and 371 DEGs were identified. By coexpression analysis, 682 lncRNA-mRNA pairs were identified with a coefficient ≥ 0.9 and p < 0.05. The ceRNA network with 8 lncRNAs, 3 miRNAs and 22 mRNAs was constructed visualized by Cytoscape. LncRNA RP11-66N24.4 and LINC00310 are among the top 10% nodes and the associated ceRNA subnetwork may be the center of the whole ceRNA network. Furthermore, the qRT-PCR results showed that LINC00310 was signifcantly decreased in HCM patients. For LINC00310, GO analysis revealed that the biological processes was enriched in cardiovascular system development, sprouting angiogenesis, circulatory system development and so on, and Pathway analysis was mainly enriched in cGMP-PKG signaling pathway. Our study reveals the novel lncRNA-related ceRNA network in HCM and the identified lncRNA LINC00310 may be roles in the pathogenesis mechanisms of HCM, which could provide further insight into the pathogenesis of HCM.
2022-09-28 | GSE197191 | GEO
Project description:Ischemic cardiomyopathy(ICM) and dilated cardiomyopathy(DCM), with distinct long-term prognosis and responses to treatment, are two major problems that lead to heart failure(HF) ultimately. In this study, we investigated the lncRNA and mRNA expressions in the plasma of patients with DCM and ICM and analyzed the different lncRNA profile between the two groups. These findings revealed for the first time the specific expression pattern of both protein-coding RNAs and lncRNAs in plasma of HF patients due to DCM and ICM which may provide some important evidence to conveniently identify the etiology of myocardial dysfunctions and help to explore a better strategy for future HF prognosis evaluation.
2022-10-08 | GSE138678 | GEO
Project description:Noncoding RNAs include small transcripts, such as microRNAs and piwi-interacting RNAs, and a wide range of long noncoding RNAs (lncRNAs). Although many lncRNAs have been identified, only a small number of lncRNAs have been characterized functionally. Here, we sought to identify lncRNAs differentially expressed during replicative senescence. We compared lncRNAs expressed in proliferating, early-passage, 'young' human diploid WI-38 fibroblasts [population doubling (PDL) 20] with those expressed in senescent, late-passage, 'old' fibroblasts (PDL 52) by RNA sequencing (RNA-Seq). Numerous transcripts in all lncRNA groups (antisense lncRNAs, pseudogene-encoded lncRNAs, previously described lncRNAs and novel lncRNAs) were validated using reverse transcription (RT) and real-time, quantitative (q)PCR. Among the novel senescence-associated lncRNAs (SAL-RNAs) showing lower abundance in senescent cells, SAL-RNA1 (XLOC_023166) was found to delay senescence, because reducing SAL-RNA1 levels enhanced the appearance of phenotypic traits of senescence, including an enlarged morphology, positive β-galactosidase activity, and heightened p53 levels. Our results reveal that the expression of known and novel lncRNAs changes with senescence and suggests that SAL-RNAs play direct regulatory roles in this important cellular process. RNA was extracted from both young and senescent WI-38 cells and used for total RNA-Seq.
2016-02-08 | E-GEOD-77675 | biostudies-arrayexpress