Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33159375_1.fastq.gz | Fastqsanger.gz | |||
| SRR33159375_2.fastq.gz | Fastqsanger.gz | |||
| SRR33159376_1.fastq.gz | Fastqsanger.gz | |||
| SRR33159376_2.fastq.gz | Fastqsanger.gz | |||
| SRR33159377_1.fastq.gz | Fastqsanger.gz |
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Project description:Arteriovenous hemodialysis graft (AVG) stenosis results in thrombosis and AVG failure, and develops chiefly as a consequence of neotinimal hyperplasia (NH) formation in the graft-venous anastomosis region. Of note, the juxta-anastomotic vein regions are relatively resistant to NH. AVG stenosis has not been resolved partly due to our limited understanding of the molecular processes involved in the pathophysiology. We hypothesized that the gene expression profiles of the NH prone and NH-resistant regions will be different after graft placement, and analysis of their genomic profiles may yield therapeutic targets to address AVG stenosis. To test this hypothesis we evaluated the global genomic profiles of the graft-venous anastomosis (NH-prone) and juxta-anastomotic (NH-resistant) vein regions in a porcine model of AVG stenosis using a porcine microarray. Gene expression changes in these two distinct vein regions, relative to the gene expression in un-operated veins, were examined at an early (5 days) and later (14 days) time period following graft placement. Global genomic changes were much greater in the NH-prone region than in the NH-resistant region at both time points. In the NH-prone region, genes related to regulation of cell proliferation and osteo/chondrogenic vascular remodeling were most enriched among the significantly up-regulated genes at day 5 and day 14, respectively. At both time points, genes related to muscle phenotype were significantly down-regulated. These results provide insights into the spatial and temporal genomic modulation underlying NH formation in AVG, and suggest potential therapeutic strategies to prevent and/or limit AVG stenosis.
2018-05-08 | GSE97377 | GEO
Project description:In mouse early pachytene spermatocytes, the X and Y chromosomes undergo rapid non-homologous (NH) synapsis and desynapsis, but the functional significance remains unknown. Here, we report that pachynema-specific knockout of Speedy A (SpdyA) from telomeres caused persistent Y-X NH synapsis, with the entire Y axis synapsed onto the X axis. This persistent Y-X NH synapsis did not interrupt meiotic sex chromosome inactivation, recombination, or sex body formation, but it disrupted X-Y loop-axis organization and homologous X-Y desynapsis, leading to spermatocyte death. Similarly, persistent Y-X NH synapsis was also observed in pachytene spermatocytes lacking TRF1, where SpdyA was frequently lost from X-Y non-pseudoautosomal region (non-PAR) telomeres. Mechanistic studies revealed that the Serine 48 of SUN1 is a key SpdyA/CDK2 phosphorylation site needed for Y-X NH desynapsis. We propose that SpdyA governs Y-X NH desynapsis by stabilizing the linkage between the X-Y non-PAR telomeres and their LINC complexes, and that this process is regulated independently from other aspects of pachynema progression. Our findings suggest a key role for Y-X NH desynapsis in establishing proper X-Y loop-axis organization.
2025-11-18 | GSE276678 | GEO
Project description:Phospholamban R14del mutazion (PLN-R14del) has been identified in a large family pedigree in which heterozygous carriers exhibited inherited dilated cardiomyopathy (DCM) and death by middle age. To better understand the causal link between the mutations in PLN and DCM pathology, we derived induced pluripotent stem cells from a DCM patient carrying the PLN R14del mutation. We showed that iPSC-derived cardiomyocytes recapitulated the DCM-specific phenotype and demonstrated that either TALEN-mediated genetic correction or combinatorial gene therapy resulted in phenotypic rescue. Our findings offer novel insights into the pathogenesis caused by mutant PLN and point to the development of potential new therapeutics of pathogenic genetic variants associated with inherited cardiomyopathies. Submitter confirms there are no patient privacy concerns with these data. iPSCs were derived from a female patient carrying a heterozygous mutation (R14del) in the PLN gene. Tree samples were analyzed: R14del-CMs (clone L2), corrected R14del-CMs (clone L2GC1) and corrected R14del-CMs (clone L2GC2)
2015-02-09 | E-GEOD-65762 | biostudies-arrayexpress
Project description:Background - Cardiac microRNAs (miRNAs) could be released into circulation thus becoming circulating cardiac miRNAs, which are increasingly recognized as noninvasive and readily accessible biomarker for multiple heart diseases. A global loss of cardiac miRNAs due to dicer or dgcr8 depletion has been reported to lead to dilated cardiomyopathy (DCM). However, DCM-associated circulating miRNAs (DACMs) and their roles in regulating DCM progression remain largely unexplored. Methods and Results - Through miRNA sequencing of human plasma procured from DCM patients and healthy control people, DCM was characterized with a unique expression pattern for circulating miRNAs. Among them, miR-26a-5p, miR-30c-5p, miR-126-5p, and miR-126-3p were all identified with dramatic reductions in DCM mouse myocardium as in the plasma of DCM patients. FOXO3, highlighted as a predicted common target gene, was experimentally demonstrated to be repressed within cardiomyocytes by these miRNAs except miR-26a-5p. Mechanistically, miRNA combination (miR-30c-5p, miR-126-5p, and miR-126-3p) significantly attenuated FOXO3-induced apoptosis and autophagy observed in cardiomyocytes as well as in DCM murine heart. Cardiac-specific knockout of FOXO3 conspicuously mitigated myocardial apoptosis and autophagy in DCM development. Moreover, stymieing the interaction between these miRNAs and FOXO3 mRNA extremely crippled the cardioprotection of these miRNAs against DCM progression. Cardiac miRNA-FOXO3 axis plays a pivotal role in safeguarding against myocardial apoptosis and autophagy, thereby maintaining cardiac homeostasis and potently preventing DCM development. These findings may provide serological clues for the noninvasive diagnosis of DCM in the future, and unambiguously shed new light on DCM pathogenesis and associated therapeutic targets
2022-07-31 | GSE209991 | GEO
Project description:We conducted chromatin immunoprecipitation followed by sequencing (ChIP-seq) and proximity ligation-assisted ChIP-seq (PLAC-seq) for enhancers and promoters (E-P) using left ventricular tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors. Differential active enhancer H3K27ac and promoter H3K4me3 regions were identified between NF and DCM. While the average read density (ARD) for H3K27ac is similar between NF and DCM, the ARD of H3K4me3 is significantly lower in DCM samples than in NF.Super-enhancer (SE) analysis revealed that 929 and 129 genes linked to NF- and DCM-specific SE, respectively, and three unique SE-associated genes between NF and DCM were identified.Moreover, the differential E-P interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. We have established cistrome of four histone modifications and long-range chromatin interaction for enhancers and promoters in NF and DCM tissues. The differential histone modifications and E-P interactions were found in DCM, and these differences were associated with the gene expression level of a subset of disease-associated genes in human heart failure.
2022-01-15 | GSE135953 | GEO
Project description:We conducted chromatin immunoprecipitation followed by sequencing (ChIP-seq) and proximity ligation-assisted ChIP-seq (PLAC-seq) for enhancers and promoters (E-P) using left ventricular tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors. Differential active enhancer H3K27ac and promoter H3K4me3 regions were identified between NF and DCM. While the average read density (ARD) for H3K27ac is similar between NF and DCM, the ARD of H3K4me3 is significantly lower in DCM samples than in NF.Super-enhancer (SE) analysis revealed that 929 and 129 genes linked to NF- and DCM-specific SE, respectively, and three unique SE-associated genes between NF and DCM were identified.Moreover, the differential E-P interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. We have established cistrome of four histone modifications and long-range chromatin interaction for enhancers and promoters in NF and DCM tissues. The differential histone modifications and E-P interactions were found in DCM, and these differences were associated with the gene expression level of a subset of disease-associated genes in human heart failure.
2022-01-15 | GSE135954 | GEO
Project description:The HCC and adjacent NH tissues were isolated from 9 HCC patients and RNA was extracted from the paired samples.
2021-02-09 | GSE166348 | GEO
Project description:Circular RNAs (circRNAs) have been reported to play important roles in various cardiovascular diseases. However, their expression profile in human dilated cardiomyopathy (DCM) has not been fully elucidated. In our study, heart samples from DCM patients and healthy controls were used to identify circRNAs by high-throughput sequencing. A total of 9585 circRNAs were identified in the DCM and control groups. To assess the differentially expressed circRNAs, the criteria were set as a fold change of ≥ 2 or ≤ 0.5 and a P value of < 0.05. Compared with circRNAs in the control group, 298 dysregulated circRNAs were identified in patients with DCM, of which 231 were upregulated and 85 were downregulated. In conclusion, our study evaluated cardiac circRNA expression in DCM by high-throughput sequencing and provide a foundation for future studies of circRNAs in DCM.
2021-03-10 | GSE162505 | GEO
Project description:To explore the unique pathogenesis of DCM and analyzed the differences in gene expression, associated pathways and immune cell infiltration among different organs that are targeted by high glucose by bioinformatics-based strategy. In order to find the specific factors that trigger DCM, we contrasted the gene profile of DCM to that of other diabetic diseases including diabetic peripheral neuropathy (DPN) and nephropathy (DN). we performed RNA-seq and miRNA sequencing on heart tissue from db/db mice to explore the transcriptome alterations in DCM pathogenesis including lncRNA, miRNA and mRNA.
2023-05-10 | GSE211107 | GEO