RNA-sequence analysis of WT mice hearts and cardiomyocyte-specific deletion of STAT3 mice hearts
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE160248 | GEO | 2023/10/12
REPOSITORIES: GEO
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Project description:RNA-sequence analysis of WT mice hearts and cardiomyocyte-specific deletion of STAT3 mice hearts
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Project description:Gene expression analysis of heart tissue probes from a mouse model with a cardiomyocyte-restricted STAT3 deficiency in comparison to corresponding WT mice. (Hilfiker-Kleiner, D. et al. 2004) Comparison of heart left ventricle tissue probes from STAT3-KO and WT mice. Each sample is a pool of 5 tissue probes from each genotype.
2011-06-30 | E-GEOD-30306 | biostudies-arrayexpress
Project description:We found that cardiomyocyte-specific PRMT1-deficient (PRMT1-cKO) mice showed dilated cardiomyopathy and aberrant cardiac alternative splicing. To identify novel cardiac splicing events, we performed a comprehensive analysis of gene expression changes in hearts of wildtype (WT) and PRMT1-cKO mice using RNA sequencing (RNA-Seq). To investigate differentially expressed genes (false discovery rate (FDR) p<0.05, fold change >2) between control and PRMT1-cKO mice, we performed pairwise comparisons of RNA-Seq data using the CLC Genomics Workbench software.
2018-09-27 | GSE112938 | GEO
Project description:Gene expression analysis of heart tissue probes from a mouse model with a cardiomyocyte-restricted STAT3 deficiency in comparison to corresponding WT mice. (Hilfiker-Kleiner, D. et al. 2004)
2011-06-30 | GSE30306 | GEO
Project description:RNA-seq analysis of hearts from control and cardiomyocyte-specific PRMT1-deficient mice
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Project description:Many patients have cancers that have increased activity of a protein called STAT3 that contributes critically to the development and growth of their cancer. Despite our knowledge of STAT3’s importance to cancer, scientists and doctors have not developed a drug that targets it and that patients can take to treat their cancer more effectively than treatments that are now available. Tvardi Therapeutics, Incorporated has developed a compound, TTI-101, which can be given by mouth and acts as a direct inhibitor of STAT3. Administration of TTI-101 to mice demonstrated that it blocked growth of cancers of the breast, head and neck, lung, and liver and it was safe when administered at high doses to mice, rats, and dogs. In this application, Tvardi is proposing to further develop TTI-101 for treatment of solid tumors for which the prognosis is dismal. The investigators will determine how safe it is when administered to patients with cancer, determine whether an adequate dose can be administered to patients with cancer that will block STAT3 in their cancer, and determine whether treatment with TTI-101 leads to reduced growth of their cancer.
| 2247646 | ecrin-mdr-crc
Project description:Genome wide gene expression analysis of mRNA siolated from whole heart tissue from wild type and cardiomyocyte selective MR null mice. The role of mineralocorticoid receptors (MR) in specific cell types of the myocardium in cardiac remodeling remains unknown. We investigated MR in cardiomyocytes in DOC/salt-induced cardiac pathology. Cardiomyocyte MR-null mice (CM-MRKO) and control mice (WT) were given DOC/salt and cardiac responses were examined at 8 days and 8 weeks. Cardiac function in untreated mice wild type and CM-MRKO mice was determined by Langendorf and showed no differences. At 8 days CM-MRKO showed equivalent monocyte/macrophage recruitment to wild type mice in response to DOC/salt treatment. Profibrotic markers were significantly reduced in CM-MRKO hearts at base line and in response to DOC/salt. In contrast, at 8 weeks CM-MRKO mice showed no DOC/salt-induced increase in inflammatory cell infiltrate, fibrosis or systolic blood pressure (SBP). Similarly, DOC/salt-mediated increases in proinflammatory and profibrotic gene expression were not detected in CM-MRKO mice. Although mRNA levels for fibronectin and collagen III were similar for each genotype, this was not translated into protein expression. Interestingly, untreated CM-MRKO mice showed increased mRNA and protein for decorin and a further increase with DOC/salt. Together, these data suggest a direct role for cardiomyocyte MR in DOC/salt-induced tissue remodelling and SBP regulation. Moreover, a specific profibrotic pathway is dysregulated in CM-MRKO mice, suggesting a potential mechanism for the cardioprotective effects of selective MR deletion in cardiomyocytes. Pool mRNA (equal amounts) from whole heart from 8 animals per group.
2013-06-30 | E-GEOD-38869 | biostudies-arrayexpress
Project description:Background: BMPER, an orthologue of Drosophila melanogaster crossveinless-2, is a secreted factor that regulates BMP activity in endothelial cell precursors and during early cardiomyocyte differentiation. Although previously described in the heart, the role of Bmper in cardiac development and function remained unknown. Methods: BMPER deficient hearts were phenotyped histologically and functionally using echocardiography and Doppler analysis. Since BMPER -/- mice die perinatally, BMPER +/- mice were then challenged to pressure overload induced cardiac hypertrophy and hind limb ischemia to determine changes in angiogensis and regulation of cardiomyocyte size. Results: We identified for the first time the cardiac phenotype associated with BMPER haploinsufficiency. BMPER mRNA and protein are present in the heart during cardiac development through at least E14.5 but is lost by E18.5. BMPER +/- ventricles are thinner and less compact than sibling wild-type hearts. In the adult, BMPER +/- hearts present with decreased anterior and posterior wall thickness, decreased cardiomyocyte size, and an increase in cardiac vessel density. Despite these changes, BMPER +/- mice respond to pressure overload-induced cardiac hypertrophy challenge largely to the same extent as wild-type mice. Conclusion: BMPER appears to play a role in regulating both vessel density and cardiac development in vivo; however, BMPER haploinsufficiency does not result in marked effects on cardiac function or adaptation to pressure overload hypertrophy. Unpaired, two-condition experiment, wild-type vs BMPER+/- adult hearts. Biological replicates: 4 per condition.
2012-09-20 | E-GEOD-40983 | biostudies-arrayexpress
Project description:We have demonstrated previously that adult cardiomyocytes can dedifferentiate and proliferate when cultured in vitro. To determine if cardiomyocyte dedifferentiation and cell cycling/proliferation happens in vivo, we applied here a novel multi-reporter transgenic mouse model (aMH-CMerCreMer;mT/MG;aMHC-H2BBFP) carrying reporter genes for permanent cardiomyocyte lineage mapping and maturity (dedifferentiation) reporting. With this new model, we deciphered the cellular sources and processes of cardiomyocyte dedifferentiation and proliferation in adult hearts. In this study, we used single-nucleus RNA-sequencing to tackle the challenges in analyzing the highly heterogeneous heart cell populations, and obtained datasets for a large number of cardiac single nuclei (both myocytes and non-myocytes) for control and post-infarct hearts. We identified specific cell populations in the heart using distinct transcriptomic clusters, transgenic reporters for ACM lineage and dedifferentiation, as well as cell cycle markers. The results demonstrated that the dedifferentiation and cell cycle progression of pre-existing CMs was augmented in post-infarct hearts, with a number of signaling pathways and gene sets affected. This is the first study dissecting the transcriptomic profiles and signaling pathways associated with cardiomyocyte dedifferentiation and cycling/proliferation in vivo using unbiased high-throughput single-nucleus RNA-Seq analysis, in junction with novel cell lineage (e.g. cardiomyocyte) and phenotyping (e.g. dedifferentiation) transgenic model systems.
2019-07-02 | GSE128628 | GEO
Project description:Purpose: To elucidate the roles of airway epithelial STAT3 in allergic airway inflammation. Method: Doxycycline-induced airway epithelial cells-specific STAT3-deficient mice (STAT3-cKO) and their genetic control mice (STAT3-WT) were sensitized intratracheally twice with house dust mite (HDM) extract or PBS at a 7-day interval. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 206 transcripts showed differential expression between HDM-treated STAT3-WT and STAT3-cKO with adjusted p value <0.05.
2022-04-01 | GSE190345 | GEO