Similar Datasets
Project description:We reported the RNAseq analyses of right ventricualr free wall myocardium in neonatal volume overload (VO) SD rat. VO was induced by the fistula between abdominal aorta and inferior vena cava (AVF) within 24 hours postnatally (P1). RNAseq analyses of RV free wall at P7 from VO and sham-operated rat revealed that there were 454 differentially expressed genes between VO and sham group at P7. GO analysis showed that in the VO and sham comparison, the upregulated genes mainly mediated immune system response and the downregulated genes mainly mediated apoptotic process at P7. VO has no effect to neonatal right ventricular cardiomyocyte proliferation.
2021-12-08 | GSE180643 | GEO
Project description:To investigate the effect of volume overload (VO) during postnatal right atrium (RA) development, we established the RA VO model by conducting the fistula between abdominal aorta and inferior vena cava (ACF) on postnatal day 7(P7) C57/BL6 mice. We then performed gene expression analysis using data obtained from RNA-seq of RA from VO and sham-operated mice at postnatal day 21 (P21).
2023-10-12 | GSE232594 | GEO
Project description:We reported the RNAseq analyses of right ventricualr free wall myocardium in young volume overload (VO) C57/BL6 mice.VO was induced by the fistula between abdominal aorta and inferior vena cava (AVF) on postnatal day 7(P7). RNAseq analyses of RV free wall at P14 and P21from VO and sham-operated mice revealed that there were 981 differentially expressed genes between VO and sham group at P14, this number increased to 1907 at P21, there were 3012 differentially expressed genes between P21 and P14 sham group, and the number increased to 3470 at the presence of VO. GO analysis showed that in the VO and sham comparison, the upregulated genes mainly mediated mitosis and cell division and the downregulated genes mainly mediated heart contraction at P14, and the upregulated genes mainly mediated immune response, and downregulated genes mainly mediated cellular respiration at P21. As expected, in the normal RV development during preadolescence (from P14 to P21), upregulated genes mainly mediated oxidative phosphorylation and cellular respiration and the downregulated genes mainly mediated vasculogenesis. VO changed the RV development, the upregulated genes mainly mediated heart contraction and the down regulated genes mainly mediated vasculogenesis and cell cycle. KEGG pathway analysis revealed that cell cycle pathway was upregulated and cardiac muscle contraction and thyroid hormone signaling pathway were downregulated between VO and sham group at P14, phagosome pathway was upregulated and citrate cycle (TCA) cycle and thermogenesis were downregulated at P21 between VO and sham group. In the normal RV development, TCA cycle and cardiac muscle contraction pathway were upregulated while VO changed that to the upregulations of cardiomyopathy pathways and thyroid hormone signaling pathway. All the above changes were further confirmed by the functional tests.
2021-08-16 | GSE157396 | GEO
Project description:We reported the RNAseq analyses of left ventricualr free wall myocardium in young volume overload (VO) C57/BL6 mice.VO was induced by the fistula between abdominal aorta and inferior vena cava (AVF) on postnatal day 7(P7). RNAseq analyses of LV free wall at P14 and P21from VO and sham-operated mice revealed that there were 378 differentially expressed genes between VO and sham group at P14, this number decreased to 184 at P21, there were 1374 differentially expressed genes between P21 and P14 sham group, and the number chenged to 1167 at the presence of VO. GO analysis showed that in the VO and sham comparison, the upregulated genes mainly mediated cell−cell junction and the downregulated genes mainly mediated regulation of immune response at P14, and the upregulated genes mainly mediated cell growth, and downregulated genes mainly mediated response to interferon−beta at P21. As expected, in the normal LV development during preadolescence (from P14 to P21), upregulated genes mainly mediated muscle system process and regulation of membrane potential and the downregulated genes mainly mediated regulation of mitotic cell cycle. VO changed the LV development, the upregulated genes mainly mediated regulation of protein catabolic process and the down regulated genes mainly mediated antigen processing and presentation. KEGG pathway analysis revealed that glucagon signaling pathway was upregulated and phagosome pathway and chemokine signaling pathway were downregulated between VO and sham group at P14, protein processing in endoplasmic reticulum was upregulated and antigen processing and presentation were downregulated at P21 between VO and sham group. In the normal LV development, calcium signaling pathway and cardiac muscle contraction pathway were upregulated while VO changed that to the arginine and proline metabolism . All the above changes were further confirmed by the functional tests.
2022-04-07 | GSE186968 | GEO
Project description:We reported the RNAseq analyses of right ventricular free wall of myocardium in three groups of mice（3 in each group）at postnatal day 14 (P14). The mice in volume overload (VO) group underwent an abdominal surgery by puncture from aorta to inferior vena cava at P7, mice in Sham group underwent the same surgery except for the puncture. The mice in CsA group were VO mice who were also injected with cyclosporin A(CsA) for seven days. The results revealed that there were differentially expressed genes between VO and sham group at P14, Inhibiting the immune response with CsA caused the gene expression profile of VO mice to shift towards that of sham mice.
2024-02-01 | GSE254207 | GEO
Project description:Genome-wide characterization of histone H4 acetylation in K562 cells in optimal growth conditions (NHS) and upon 30 min heat stress at 42°C (HS30).
2017-05-21 | GSE89382 | GEO
Project description:HSF1 binds DNA via the DBD domain, causing gene upregulation during HS. We assessed the effect of RD-mediated phase separation on chromatin targeting of HSF1 using Cut&Tag followed by high-throughput sequencing to map genome-wide binding of LLPS-competent versus LLPS-incompetent HSF1 mutants under both HS and NHS conditions. Comparing with WT HSF1 under NHS, both WT under HS and M1 under NHS showed increased and broad binding to enhancers and distal intergenic region, with binding most enriched in expected motifs of HSF-related transcription factors. To further assess the role for IDR-induced LLPS in chromatin targeting of HSF1, we used several additional strategies. First, the treatment of 1,6-hexanediol markedly decreased chromatin occupancy both of WT under HS and M1 under NHS conditions. Second, we interrogate chromatin binding of LLPS-deficient mutant M3. Cut&Tag analysis revealed that M3 showed decreased chromatin binding compared to WT under HS and M1 under NHS. The decreased chromatin binding of M3 to chromatin was not due to the loss of its DNA binding ability, as the EMSA assay revealed that M3 was still capable of binding HSE. Instead, the decreased chromatin binding reflects the loss of inter-molecular interaction between HSF1 that holds LLPS. Furthermore, M3 in heat shocked cells shows similar reduced genomic targeting and shallow binding pattern as NHS cells . Third, the enrichment of transcriptional apparatus RNA Pol II, CYCT1, BRD4 to HSF1 target genes also depend on whether HSF1 can phase separate at these sites. Lastly, we conducted live cell single molecule imaging to evaluate chromatin binding kinetics of LLPS-deficient mutant M3 relative to WT HSF1. Measurements of single molecule displacement and diffusion coefficient showed M3 to be significantly more mobile than WT under HS, which suggests M3 was less confined within phase-separated puncta compared with LLPS-competent HSF1. Consistent with this result, super resolution imaging of M3 also showed decreased cluster formation at HSP gene foci but maintained nSBs formation. Altogether, LLPS-forming capability of HSF1 is essential for the efficient recruitment of HSF1 and transcriptional apparatus to HSP gene loci.
2021-12-24 | GSE192370 | GEO