Project description:To capture the swift changes in gene expression upon INO80-OE, we performed time-coursed (D0, D2, D4, and D6) RNA sequencing (RNA-Seq) following INO80 induction.
Project description:We carried out bulk RNA sequencing of normal adult mouse CMs (Control-CMs) and adult mouse CMs with ectopic overexpression of Yamanaka factors (Oct4, Sox2, Klf4, Myc, OSKM-CMs), based on a hypothesis that OSKM would induce at least partial CM dedifferentiation in vivo. More than 2,000 genes were differentially expressed between Control- and OSKM-CMs, which were enriched for gene ontology (GO) terms related to multiple key aspects of CM dedifferentiation. This study provides a genome-wide transcriptional profile of dedifferentiating CMs induced by OSKM.
Project description:Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage. To test the identity and the degree of differentiation of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. Global gene expression profiles by microarray was obtained in c-kitpos eCSCs, c-kitpos eCSC-derived YFPpos CMs and normal adult CMs. c-kitposCD45neg eCSCs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice and harvested at 4th passage (n=3). YFPpos cardiomyocytes were FACS sorted from left ventricle apex of Lentirius-c-kit/cre recombined B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice 28 days after ISO (N=3). Normal adult CMs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice (n=3).
Project description:Transcriptional regulatory circuits that drive cardiomyocyte maturation are poorly understood. Human iPS cell-derived cardiomyocytes (hiPSC-CMs) have been shown to have fetal cardiomyocyte features in terms of metabolic gene expression profiles. Here we found that in hiPSC-CMs, overexpression of estrogen-related receptor gamma (ERRg) is sufficient to drive cardiomyocyte metabolic maturation programs including the induction of a number of oxidative mitochondrial metabolic genes.
Project description:Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage.
Project description:The use of single cell RNA sequencing (scRNA-seq) remains limited in cardiac pathology owing to technical difficulties associated with the isolation of single adult cardiomyocytes (CMs). Here, we investigated the capability of large-particle fluorescence-activated cell sorting (LP-FACS) for isolation of viable single adult CMs. We found that LP-FACS readily outperforms conventional FACS for isolation of structurally competent CMs, including large CMs. Additionally, LP-FACS enables isolation of fluorescent CMs from mosaic models. Importantly, the sorted CMs allow generation of high-quality scRNA-seq libraries. Unlike CMs isolated via previously utilized fluidic or manual methods, LP-FAC-isolated CMs generate libraries exhibiting normal levels of mitochondrial transcripts. Moreover, LP-FACS isolated CMs remain functionally competent and can be studied for contractile properties.
Project description:ChIP assay was performed to study the genomic location of SRF myocytes cistrome in adult ventricular cardiomyocytes. The myocytes were stimulated by phenylephrine (PE) combined with adenoviral overexpression of SRF serine-103 mutants.