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Activation of Hydroxy-carboxylic Acid Receptor 1 effect on cardiomyocytes

ABSTRACT: Activation of Hydroxy-carboxylic Acid Receptor 1 effect on cardiomyocytes

PROVIDER: PRJNA932761 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23372092_1.fastq.gz	Fastqsanger.gz
	SRR23372092_2.fastq.gz	Fastqsanger.gz
	SRR23372093_1.fastq.gz	Fastqsanger.gz
	SRR23372093_2.fastq.gz	Fastqsanger.gz
	SRR23372094_1.fastq.gz	Fastqsanger.gz

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Activation of Hydroxy-carboxylic Acid Receptor 1 effect on cardiomyocytes

Project description:Our aim is to explore the effect of Hydroxy-carboxylic Acid Receptor 1 on cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured. Subsequently, NRCMs were treated with the agonist of Hydroxy-carboxylic Acid Receptor 1 (HCAR1), 3Cl-HBA at 40 μM for 48 h(HBA1,HBA2 and HBA3) or DMSO as control(C1,C3 and C3). RNA was extracted using the KAPA RiboErase RNA-Seq kit (Roche, Basel, Switzerland), and was analysed using the Agilent Bioanalyzer 2100 system (Agilent Technologies, CA, USA) for quality control. The libraries were sequenced on an Illumina HiSeq X Ten platform. DESeq2 was used to analyse RNA-seq data. Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured. Subsequently, NRCMs were treated with the agonist of Hydroxy-carboxylic Acid Receptor 1 (HCAR1), 3Cl-HBA (40 μM for 48 h) or DMSO as control. RNA was extracted using the KAPA RiboErase RNA-Seq kit (Roche, Basel, Switzerland), and was analysed using the Agilent Bioanalyzer 2100 system (Agilent Technologies, CA, USA) for quality control. The libraries were sequenced on an Illumina HiSeq X Ten platform.

2024-02-14 | GSE224822 | GEO

Early N-hydroxy-pipecolic acid transcriptional profile

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Am80 activates cardiomyocytes cell cycle via retinoic acid receptor for efficient transplantation

Project description:Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-cardiomyocytes) are promising sources for the regenerative therapy to treat heart failure. To realize this therapy, the engraftment potential of hiPSC-cardiomyocytes following the injection into the host heart should be improved. Here, we established the efficient method to analyze the cell cycle activity of hiPSC-cardiomyocytes using Fluorescence Ubiquitination-based Cell Cycle Indicator (FUCCI) system. High-throughput screening analysis using FUCCI-expressing hiPSC-cardiomyocytes identified a retinoic acid receptor (RAR) agonist, Am80, as an effective cell cycle activator in hiPSC-cardiomyocytes. The transplantation of hiPSC-cardiomyocytes treated by Am80 prior to the injection significantly enhanced the engraftment into the damaged mouse heart for 6 months. RNA sequencing analysis in Am80-treated iPSC-cardiomyocytes revealed that both RARA and RARB played important roles in the Am80-mediated cell cycle activation in hiPSC-cardiomyocytes. Collectively, this study highlights the effectiveness of FUCCI system to easily analyze the cell cycle status in hiPSC-cardiomyocytes and the cell cycle activation by Am80 is the possible strategy to increase the graft size following the cell transplantation into the damaged heart.

2023-07-12 | GSE176303 | GEO

Am80 activates cardiomyocytes cell cycle via retinoic acid receptor for efficient transplantation

Project description:Am80 activates cardiomyocytes cell cycle via retinoic acid receptor for efficient transplantation

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Early N-hydroxy-pipecolic acid transcriptional profile

Project description:N-hydroxy-pipecolic acid (NHP) is a mobile metabolite essential for inducing and amplifying systemic acquired resistance (SAR) following pathogen attack. In Arabidopsis thaliana (Arabidopsis), exogenous NHP is sufficient to activate SAR-related immune responses, including salicylic acid (SA) accumulation and changes in global transcriptional profile. Previous studies have tracked these changes 1-2 days after an initial NHP treatment, resulting in little knowledge of the very early phases of NHP signaling and transcriptional responses leading to immunity. Here we show NHP elicits transcriptional changes within minutes of treatment. We report distinct waves of expression over the course of minutes to hours defined by transient induction of jasmonic acid/wound-related responses, a primary induction of WRKY transcription factor expression, and subsequent induction of WRKY-regulated defense genes. The upregulation of WRKYs and the majority of defense-related genes occurred in the sid2-2 mutant, which is unable to accumulate SA upon NHP treatment, suggesting NHP is sufficient to drive the early phase of transcriptional changes in a low SA environment. We also show that WRKY70 is required for the expression of a set of genes defining the secondary transcriptional changes, as well as NHP enhancement of ROS production and SAR.

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Project description:Hydroxylated fatty acids are important intermediates in lipid metabolism and signaling. Surprisingly, the metabolism of 4-hydroxy fatty acids remains largely unexplored. We found that both ACAD10 and ACAD11 unite two enzymatic activities to introduce these metabolites into mitochondrial and peroxisomal β-oxidation, respectively. First, they phosphorylate 4-hydroxyacyl-CoAs via a kinase domain, followed by an elimination of the phosphate to form enoyl-CoAs catalyzed by an acyl-CoA dehydrogenase (ACAD) domain. Studies in knockout cell lines revealed that ACAD10 preferentially metabolizes shorter chain 4-hydroxy fatty acids than ACAD11 (i.e. 6 carbons versus 10 carbons). Yet, recombinant proteins showed comparable activity on the corresponding 4-hydroxyacyl-CoAs. This suggests that the localization of ACAD10 and ACAD11 to mitochondria and peroxisomes, respectively, might influence their physiological substrate spectrum. Interestingly, we observed that ACAD10 is cleaved internally during its maturation generating a C-terminal part consisting of the ACAD domain, and an N-terminal part comprising the kinase domain and a haloacid dehalogenase (HAD) domain. HAD domains often exhibit phosphatase activity, but negligible activity was observed in the case of ACAD10. Yet, inactivation of a presumptive key residue in this domain significantly increased the kinase activity, suggesting that this domain might have acquired a regulatory function to prevent accumulation of the phospho-hydroxyacyl-CoA intermediate. Taken together, our work reveals that 4-hydroxy fatty acids enter mitochondrial and peroxisomal fatty acid β-oxidation via two enzymes with an overlapping substrate repertoire.

2024-09-13 | PXD050316 | Pride

Genome-wide estrogen-related receptor gamma (ERRg) occupancy in human iPS cell-derived cardiomyocytes (hiPSC-CMs)

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