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Transcriptional profile of injured hearts treated with the cholinesterase inhibitor pyridostigmine (PYR) at Day 5

ABSTRACT: Transcriptional profile of injured hearts treated with the cholinesterase inhibitor pyridostigmine (PYR) at Day 5

PROVIDER: PRJNA480795 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7514200.fastq.gz	Fastqsanger.gz
	SRR7514210.fastq.gz	Fastqsanger.gz
	SRR7514201.fastq.gz	Fastqsanger.gz
	SRR7514211.fastq.gz	Fastqsanger.gz
	SRR7514202.fastq.gz	Fastqsanger.gz

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Transcriptional profile of injured hearts treated with the cholinesterase inhibitor pyridostigmine (PYR) at Day 5

Project description:It has been shown that acetylcholine has anti-inflammatory properties. The aim of this study is to investigate the role of acetylcholine in cardiac inflammation. We used the diphtheria toxin (DT)-cardiomyocyte ablation model (DTR model) (Lavine et al., 2014 - PNAS) to induce cardiac injury (DT, 2 days, 2.5µg/kg, IP). Beginning one week prior to DT injury, mice were treated with vehicle (PBS, phosphate buffered saline) or the cholinesterase inhibitor pyridostigmine (PYR, 3mg/kg, SQ). Hearts were harvested at Day 5 post-DT-injury. Here, we provide the transcriptional profile of wild-type/PBS, wild-type/PYR, DTR/PBS and DTR/PYR hearts.

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Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

Project description:Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

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P493-6 treated with KJ-Pyr-9 and/or Doxycycline

Project description:In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing human cancer cells.

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P493-6 treated with KJ-Pyr-9 and/or Doxycycline

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Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

Project description:Myocardial CD19+CD11b+ and CD19+CD11b- cells were FACS sorted from transgenic mice expressing the Diphtheria Toxin (DT) receptor under the myocardial specific MLC2v promoter. Cells were sorted from hearts of mice not exposed to DT (naïve hearts), from the hearts of animals treated with DT 4 days prior to the experiment (DTR) and from the hearts of mice exposed to DT and fed chow enriched with the anti-inflammatory/anti-fibrotic drug Pirfenidone (0.5% in powdered chow, PFD)

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