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Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

ABSTRACT: Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

PROVIDER: PRJNA1095836 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28538644_1.fastq.gz	Fastqsanger.gz
	SRR28538644_2.fastq.gz	Fastqsanger.gz
	SRR28538645_1.fastq.gz	Fastqsanger.gz
	SRR28538645_2.fastq.gz	Fastqsanger.gz
	SRR28538646_1.fastq.gz	Fastqsanger.gz

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Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

Project description:Retinoic acid (RA), the major active metabolite of vitamin A, is essential for organogenesis, homeostasis, and tissue morphogenesis. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. For a comprehensive transcriptional evaluation of the effect of RA signaling on neonatal cardiomyocyte cell cycle arrest and maturation, we performed RNA-seq analysis of cultured perinatal cardiomyocytes treated with all-trans retinoic acid (ATRA) in vitro.

2024-08-13 | GSE263096 | GEO

Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation

Project description:Retinoic acid (RA), the major active metabolite of vitamin A, is essential for organogenesis, homeostasis, and tissue morphogenesis. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. To analyze the function of RA signaling during perinatal heart development, we investigated the mRNA expression levels of multiple retinoid metabolic genes at various perinatal stages using RNA-seq analysis.

2024-08-13 | GSE263095 | GEO

Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation

Project description:Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation

| PRJNA1095834 | ENA

Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

Project description:Transcriptional profiling of human leukemia　HL-60 cells comparing ATRA treated HL-60 cells with ATRA plus ATO. Goal was to determine the effects of ATO on ATRA induced differentiation of HL-60 cells.

2015-03-31 | GSE67420 | GEO

Expression data from ATRA-treated endometrial stromal cells

Project description:Decidualization is critical for the embryonic implantation and successful pregnancy. ATRA can suppress in-vitro decidualization of human endometrial stromal cells (hESCs) induced by MPA and estrogen treatment. However, the mechanism by which RA suppressed estrogen and progesterone induced decidualization of mESCs is not clear. We used microarrays to investigate the mechanism by which all-trans RA (ATRA) regulates the decidualization of endometrial stroma cells (mESCs).

2013-11-05 | GSE52033 | GEO

Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

Project description:Transcriptional profiling of human leukemia?HL-60 cells comparing ATRA treated HL-60 cells with ATRA plus ATO. Goal was to determine the effects of ATO on ATRA induced differentiation of HL-60 cells. Two-condition experiment, ATRA vs. ATRA plus ATO treated HL-60 cells.

2015-03-31 | E-GEOD-67420 | biostudies-arrayexpress

Expression data from ATRA-treated endometrial stromal cells

2013-11-05 | E-GEOD-52033 | biostudies-arrayexpress

In vivo gene signature of TLR3KO mice stimulated by ethanol (EtOH) or all trans retinoic acid (atRA) treatment

Project description:How developmental programs reactivate in regeneration is a fundamental question in biology. We addressed this question through the study of Wound Induced Hair follicle Neogenesis (WIHN), an adult organogenesis model where stem cells regenerate entirely new hair follicles de novo following deep wounding. The exact mechanism is uncertain. Here we show that self-noncoding dsRNA activates the anti-viral receptor TLR3 to induce intrinsic retinoic acid (RA) synthesis in a gradient that predicts new hair follicle formation after wounding in mice. Additionally, in humans, rejuvenation lasers induce gene expression signatures for dsRNA and RA, with measurable increases in intrinsic RA synthesis. These results demonstrate a novel stimulus for retinoic acid synthesis by non-coding dsRNA, relevant to their broad functions in development and immunity. The goal of this experiment is to investigate the profile of gene expression rescued by atRA in TLR3KO mice.

2019-05-22 | GSE128408 | GEO

Murine embryonic stem cells synthesize retinoic acid to promote their own spontaneous differentiation

Project description:Embryonic stem cells (ESC) are derived from blastocyst-stage embryos and are thought to be functionally equivalent to the inner cell mass in their developmental potential. ESCs pluripotency is maintained through a complex interplay of different signaling pathways and a network of transcription factors, which is centered around Oct3/4, Sox2 and Nanog. Although, in general, much is known about this pluripotency self-renewal circuitry, the molecular events that lead ESC to exit from pluripotency and begin differentiation are currently less known. Retinoic acid, an active metabolite of the vitamin A (retinol), plays important and pleiotropic roles in vertebrate embryonic development and ESC differentiation. Here we demonstrate that RA promotes early steps of ESC differentiation, and that ESC increase their capacity to synthesize RA during spontaneous differentiation as embryoid bodies, up-regulating the RA biosynthetic pathway components RDH1, RDH10, ADH3, RALDH2, and CRABP2. Microarray derived from total RNA of mESC not treated or treated with all-trans retinoic acid (ATRA) for 2 hours.

2016-02-10 | E-GEOD-66043 | biostudies-arrayexpress

Impaired retinoic acid (RA) signal leads to RARbeta2 epigenetic silencing and RA resistance.

Project description:Resistance to the growth-inhibitory action of retinoic acid (RA), the bioactive derivative of vitamin A, is common in human tumors. One form of RA resistance has been associated with silencing and hypermethylation of the retinoic acid receptor beta2 gene (RARbeta2), an RA-regulated tumor suppressor gene. The presence of an epigenetically silent RARbeta2 correlates with lack of the RA receptor alpha (RARalpha). Normally, RARalpha regulates RARbeta2 transcription by mediating dynamic changes of RARbeta2 chromatin in the presence and absence of RA. Here we show that interfering with RA signal through RARalpha (which was achieved by use of a dominant-negative RARalpha, by downregulation of RARalpha by RNA interference, and by use of RARalpha antagonists) induces an exacerbation of the repressed chromatin status of RARbeta2 and leads to RARbeta2 transcriptional silencing. Further, we demonstrate that RARbeta2 silencing causes resistance to the growth-inhibitory effect of RA. Apparently, RARbeta2 silencing can also occur in the absence of DNA methylation. Conversely, we demonstrate that restoration of RA signal at a silent RARbeta2 through RARalpha leads to RARbeta2 reactivation. This report provides proof of principle that RARbeta2 silencing and RA resistance are consequent to an impaired integration of RA signal at RARbeta2 chromatin.

| S-EPMC1291229 | biostudies-literature

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