E11.5 Hand1 myocardial knockout RNA-Seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA528178 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8755790.fastq.gz | Fastqsanger.gz | |||
| SRR8755791.fastq.gz | Fastqsanger.gz | |||
| SRR8755792.fastq.gz | Fastqsanger.gz | |||
| SRR8755793.fastq.gz | Fastqsanger.gz | |||
| SRR8755794.fastq.gz | Fastqsanger.gz |
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Project description:Aims: To examine the role of the basic Helix-loop-Helix (bHLH) transcription factor HAND1 in embryonic and adult myocardium. Methods and Results: Hand1 is expressed within the cardiomyocytes of the left ventricle (LV) and myocardial cuff between embryonic days (E) 9.5-13.5. Hand gene dosage plays an important role in ventricular morphology and the contribution of Hand1 to congenital heart defects requires further interrogation. Conditional ablation of Hand1 was carried out using either Nkx2.5 knockin Cre (Nkx2.5Cre) or a-myosin heavy chain Cre (aMhc-Cre) driver. Interrogation of transcriptome data via Ingenuity Pathway Analysis (IPA) reveals several gene regulatory pathways disrupted including translation and cardiac hypertrophy-related pathways. Embryo and adult hearts were subjected to histological, functional and molecular analyses. Myocardial deletion of Hand1 results in morphological defects that include cardiac conduction system defects, survivable interventricular septal defects (VSDs), and abnormal LV papillary muscles (PM). Resulting Hand1 conditional mutants are born at Mendelian frequencies; but the morphological alterations acquired during cardiac development result in, the mice developing diastolic heart failure. Conclusions: Collectively, these data reveal that Hand1 contributes to the morphogenic patterning and maturation of cardiomyocytes during embryogenesis and although survivable, indicate a role for Hand1 conduction system and papillary morphogenesis.
2019-06-01 | GSE128571 | GEO
Project description:pcDNA3-HAND1-his was transfected into HEK293T cells and harvested after 48 hours. IMAC was carried out under denaturing conditions to enrich for HAND1,and samples were loaded onto SDS-PAGE gel with HAND1 gel band excised and submitted to LC-MS/MS.
2020-12-18 | PXD022407 | Pride
Project description:Hand1 and Hand2 are transcriptional factors, and knockout mice of these genes show left and right ventricular hypoplasia, respectively. However, their function and expression in human cardiogenesis are not well studied. To delineate their expressions and assess their functions in human cardiomyocytes (CMs) in vitro, we established two triple reporter human induced pluripotent stem cell lines, HAND1mCherry, HAND2EGFP, with MYH6-driven iRFP670 or constitutive tagBFP expression and investigated their expression dynamics during cardiac differentiation. On day 5 of the differentiation, HAND1 expression marked cardiac progenitor cells. We profiled the CM subpopulations on day 20 with RNA-sequencing and found that mCherry+ CMs showed higher proliferative ability than mCherry- CMs and identified CD105 as a surface marker of highly proliferative CMs. Finally, we revealed that LEF1 is a key regulator of proliferation and is repressively regulated by HAND1 and HAND2.
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Project description:Analysis of gene expression in SLMAP3 knockout e11.5 embryos
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Project description:The development of vertebrate extremities is a complex process which requires a highly coordinated network of different transcriptional activities. The homeodomain transcription factor Shox2 is a key player in limb formation controlling neural, muscular and skeletal development. Here, we compared gene expression profiles of wildtype and Shox2 knockout limbs using microarray experiments to identify Shox2 target genes. Forelimbs of E11.5 mouse embryos were dissected and genotyped for RNA extraction. RNA from 3-4 embryos of 2 different pregnancies was used for hybridisation to 2 arrays per genotype (wildtype and Shox2 knockout) and compared.
2014-01-16 | E-GEOD-51523 | biostudies-arrayexpress
Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs cardiomyocyte regeneration or promotes maladaptive remodeling, leading to compromised cardiac function.
2024-12-02 | E-MTAB-14508 | biostudies-arrayexpress
Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte (CM) proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.
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Project description:To investigate the signal communication from the endocardium to the trabecular myocardium, we performed single cell RNA sequencing (scRNA-seq) in E11.5 Hdac3 Tie2 knockout hearts and littermate control hearts
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Project description:Targeted deletion of skNAC in mice resulted in early embryonic lethality with cardiac defects. In order to investigate the molecular mechanism of the cardiac defect, we designed the microarray comparing gene expression of the mutant E11.5 heart to wild type E11.5 heart. Keywords: genetic modification in mouse
2010-11-19 | GSE5841 | GEO
Project description:Congenital heart disease (CHD) affects nearly 1% of births annually, and neonatal and perinatal outcomes in cases of CHD are strongly impacted by pregnancy outcomes. CHD pregnancies carry increased risk of developing pathologies of abnormal placentation including fetal growth restriction, preeclampsia, preterm birth, and stillbirth. HAND1 is a gene associated with CHD. In this study, we aimed characterize the mechanistic impacts of disrupting HAND1 on human placenta trophoblast cell lines.
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