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

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

PROVIDER: PRJNA449679 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6983700.fastq.gz	Fastqsanger.gz
	SRR6983710.fastq.gz	Fastqsanger.gz
	SRR6983720.fastq.gz	Fastqsanger.gz
	SRR6983730.fastq.gz	Fastqsanger.gz
	SRR6983701.fastq.gz	Fastqsanger.gz

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Similar Datasets

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)

2018-12-25 | GSE112984 | GEO

Genome wide gene expression analysis of acutely injured primary mouse neurons

Project description:Genome wide gene expression analysis of acutely injured primary mouse neurons

| PRJNA436989 | ENA

Mesothelioma xenografts in nude mice: PBS treated versus pirfenidone treated

Project description:Background: Malignant mesothelioma is an aggressive cancer with poor prognosis. It is characterized by prominent extracellular matrix, mesenchymal tumor cell phenotypes and chemoresistance. In this study, the ability of pirfenidone to alter mesothelioma cell proliferation and migration as well as mesothelioma tumor microenvironment was evaluated. Pirfenidone is an anti-fibrotic drug used in the treatment of idiopathic pulmonary fibrosis and has also anti-proliferative activities. Aims: Transcriptional profiling using RNA sequencing of human mesothelioma xenograft tumors treated with PBS or pirfenidone. Aim was to compare extracellular matrix and fibrosis related genes. Results: Treatment of mice harboring mesothelioma xenografts with pirfenidone alone did not reduce tumor proliferation in vivo. However, pirfenidone modified the tumor microenvironment by reducing the expression of extracellular matrix associated genes. In addition, GREM1 expression was downregulated by pirfenidone in vivo. Conclusion: By reducing two major upregulated pathways in mesothelioma and by targeting tumor cells and the microenvironment pirfenidone may present a novel anti-fibrotic and anti-cancer adjuvant therapy for mesothelioma.

2018-12-14 | GSE113803 | GEO

RNA-Seq of injured mouse hearts depleted for myofibroblast Yap [I]

Project description:RNA-Seq of injured mouse hearts depleted for myofibroblast Yap [I]

| PRJNA685438 | ENA

Bulk RNA-seq dataset of uninjured vs injured larval zebrafish hearts at 48 hours post injury on 5 days post fertilisation

Project description:This experiment sought to understand the transcriptomic changes that occur in the larval zebrafish heart following injury. 600 hearts were laser injured at 3 days post fertilisation, extracted 48 hours later and pooled into three groups of 200. RNA was extracted from the whole heart(s) and sent for sequencing along with 3 groups of 200 uninjured hearts, extracted and processed identically. RNA sequencing, quality control and alignment was performed by the commercial company GENEWIZ.

2021-10-01 | E-MTAB-10860 | biostudies-arrayexpress

Transcription profiling of injured mouse hearts from C57Bl/6 and MRL sampled at 3 time points to investigate the regenerative capacity of the mammalian heart

Project description:Previous studies have suggested that the heart may be capable of limited repair and regeneration in response to a focal injury while other studies indicate that the mammalian heart has no regenerative capacity. To further explore this issue, we performed a series of superficial and transmural myocardial injuries in C57BL/6 and MRL/MpJ adult mice. At defined time intervals following the respective injury (Days 3, 14, 30 and 60) we examined cardiac function using echocardiography, morphology, FACS cell sorting for BrdU positive cells and molecular signature using microarray analysis. We observed complete restoration of myocardial function in the superficial MRL cryoinjured heart and significantly less scar formation as compared to the injured hearts of C57BL/6 mice. Following a severe transmural myocardial injury, the MRL mouse has increased survival and decreased ventricular remodeling compared to the C57BL/6 mouse but without evidence of significant regeneration. The cytoprotective program observed in the severely injured MRL heart is in part due to increased vasculogenesis and decreased apoptosis that limits the extension of the injury. We conclude that C57BL/6 and MRL injured hearts have evidence of limited myocardial regeneration, in response to superficial injury, but the improved function and survival observed in the MRL mouse heart following severe injury is not due to significant regenerative processes. Mouse hearts from C57BL/6 and MRL/MpJ strains were injured with LAD ligation and harvested at 3, 30 and 60 days after treatement.

2007-11-23 | E-GEOD-4710 | biostudies-arrayexpress

Determining the Injury-Associated Microbial Nutrients that Facilitate Secondary Bacterial Infection in Acutely Injured Lungs

Project description:Determining the Injury-Associated Microbial Nutrients that Facilitate Secondary Bacterial Infection in Acutely Injured Lungs

| PRJNA1167754 | ENA

Heterogeneous macrophage activation in injured skeletal muscle

Project description:Macrophages are the predominant inflammatory cells during skeletal muscle injury repair. They are required for the complete repair of acutely injured skeletal muscle, but detrimentally contribute to the pathological progression of dystrophic muscle in Duchenne muscular dystrophy (DMD) patients and DMD mouse model mdx5cv mice. The cellular and molecular mechanism underlying this difference has yet to be fully elucidated. To this end, the present study compared the single-cell transcriptomes of intramuscular monocytes/macrophages from uninjured and acutely injured quadriceps of 14 weeks-old wild-typed (WT) mice, and from quadriceps and diaphragm of age-matched mdx5cv mice, using single cell-based RNA sequencing (scRNA-seq) analysis. Our results identified multiple functionally diverse monocyte/macrophage clusters co-existing in each injured muscle sample. Both Ly6Chi and Ly6Clo intramuscular monocytes/macrophages were heterogenous, containing different clusters among different injury conditions. These clusters did not conform to strict M1/M2 activation, and were involved differentially in inflammation, extracellular matrix (ECM) remodeling, and myogenesis during skeletal muscle injury repair. These findings uncovered the heterogeneity of monocyte/macrophage activation in both acutely injured and dystrophic skeletal muscle, shedding light on the molecular and cellular mechanisms underlying the differential roles of monocytes/macrophages in acute skeletal muscle injury and muscular dystrophy in DMD.

2025-06-14 | GSE270031 | GEO

RNA-seq of injured mouse hearts depleted for myofibroblast Yap and Wwtr1

Project description:RNA-seq of injured mouse hearts depleted for myofibroblast Yap and Wwtr1

| PRJNA686945 | ENA

Redundant effects of Pirfenidone against fibroblast activation and severe fibrotic lung disease

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a progressive chronic lung disease characterized by excess deposition of extracellular matrix (ECM) proteins in the lung. TGFα is a is a ligand for the epidermal growth factor receptor, and found elevated in several fibrotic lung diseases including IPF. Notably, lung-specific overexpression of TGFα alone in adult mice can cause progressive and extensive adventitial and subpleural fibrosis similar to IPF. Pirfenidone, an FDA approved drug has been shown to improve the decline in lung function in IPF patients. However, the mechanism of action of pirfenidone largely unknown. In the current study, we investigated the effects of pirfenidone using a mouse model of TGFα-induced pulmonary fibrosis and fibroblasts isolated from IPF lungs. Total lung transcriptome analysis suggest a significant overlap in dysregulated gene transcripts between TGFα model and IPF. In vivo studies demonstrate a significant improvement in lung function with pirfenidone therapy compared to vehicle-treated TGFα mice on Dox for six wks. However, pirfenidone treatment did not affect fibroproliferation, myofibroblast transformation, and ECM deposition during TGFα-induced pulmonary fibrosis. In summary, pirfenidone treatment improved lung function but had a limited or no effect on the expression of collagen, ECM genes, fibroproliferation and migration of lung-resident fibroblasts.

2022-06-01 | GSE199034 | GEO

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