Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385604 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:High throughput single-cell whole transcriptome analysis of induced cardiomyocytes during direct cardiac reprogramming [RNA-seq]
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Project description:High throughput single-cell whole transcriptome analysis of induced cardiomyocytes during direct cardiac reprogramming [Bulk-seq]
| PRJNA385605 | ENA
Project description:Analysis of induced cardiomyocytes during direct cardiac reprogramming
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Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
2007-06-30 | GSE7162 | GEO
Project description:Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.
2025-10-11 | GSE267468 | GEO
Project description:Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.
2025-10-11 | GSE267466 | GEO
Project description:Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.
2025-10-11 | GSE267464 | GEO
Project description:Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.
2025-10-11 | GSE267381 | GEO
Project description:Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.
2025-10-11 | GSE267380 | GEO
Project description:Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.
2025-10-11 | GSE267198 | GEO