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Inhibition of Fap Promotes Cardiac Repair by Stabilizing BNP

ABSTRACT: Inhibition of Fap Promotes Cardiac Repair by Stabilizing BNP

PROVIDER: PRJNA767326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16117490_1.fastq.gz	Fastqsanger.gz
	SRR16117490_2.fastq.gz	Fastqsanger.gz
	SRR16117491_1.fastq.gz	Fastqsanger.gz
	SRR16117491_2.fastq.gz	Fastqsanger.gz
	SRR16117492_1.fastq.gz	Fastqsanger.gz

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Inhibition of Fap Promotes Cardiac Repair by Stabilizing BNP

Project description:Inhibition of fibroblast activation protein promotes cardiac repair by stabilizing brain natriuretic peptide after myocardial infarction

2023-01-26 | GSE184986 | GEO

Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction

Project description:Background. Accumulation of extracellular matrix in the myocardium attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Connective tissue growth factor (CTGF) is a matricellular protein that has been shown to promote development of cardiac fibrosis. Objectives. To investigate for the potential of CTGF monoclonal antibody (CTGF mAb) in protecting from development of cardiac fibrosis following myocardial infarction (MI), and to evaluate its effect during infarct repair and acute cardiac ischemia-reperfusion (I/R) injury. Methods. Mice were subjected to MI or to I/R injury and treated with either control IgG or CTGF mAb. Cultured human cardiac fibroblasts were used to investigate the signalling mechanisms modulated by CTGF mAb. Results. Treatment with CTGF mAb for four days from day three after MI improved survival, attenuated infarct expansion, and resulted in better preserved left ventricular (LV) systolic function. CTGF mAb therapy for six weeks from day seven after MI reduced the MI-induced increase in cardiomyocyte size, heart weight to body weight ratio and remote LV fibrosis. RNA sequencing analysis of LV samples showed that CTGF mAb induced expression of cardiac repair/developmental genes and normalized the MI-induced increase in expression of inflammatory/profibrotic genes. CTGF mAb induced c-Jun N-terminal kinase (JNK) phosphorylation in vivo and in vitro, and inhibition of JNK abrogated the reduced collagen production in CTGF mAb treated fibroblasts. Conclusions. Treatment with CTGF mAb induces expression of cardiac repair/developmental genes and inhibits expression of inflammatory/pro-fibrotic genes in MI hearts providing benefit during post-MI cardiac repair and reducing post-MI cardiac fibrosis.

2019-04-02 | GSE129134 | GEO

Transcriptomic profiling of FAP+ fibroblasts

Project description:FAP+ cells had been reported to be present only in healing wounds and at sites of tissue remodelling. We have found FAP+ cells in many normal tissues and aimed to investigate whether these cells were related or whether FAP is upregulated in response to an external stimulus on a variety of cells. Furthermore we wanted to investigate whether FAP+ cells are simply fibroblasts and so compared their transcriptomic profiles to that of a typical fibroblastic population, the murine embryonic fibroblast. FAP+ cells were sorted from two mesenchymal tissues, visceral adipose and skeletal muscle, and from an epithelial organ, the pancreas. These were compared to MEFs. Cells were isolated in duplicate experiments and these were analysed separately. These were compared to previously published publically available CD4+ T-cell subset data.

2013-07-15 | E-GEOD-39438 | biostudies-arrayexpress

Long Noncoding RNA LncBAR Enhances BRG1 Protein to Promote Cardiomyocyte Cell Cycle Progression and Cardiac Repair

Project description:The mammalian heart retains regenerative capacity during the early postnatal period, but this ability declines as it matures. Enhancing cardiomyocyte proliferation represents a key therapeutic approach to promote heart regeneration and repair, yet the molecular mechanisms remain elusive. Here, we identified LncBAR (BAF complex-associated lncRNA) as a critical regulator of cardiac regeneration. LncBAR expression declines during heart development but is upregulated following cardiac injury. Loss of LncBAR impairs cardiomyocyte growth, suppresses cell cycle gene expression, and diminishes heart regeneration, as evidenced by reduced cytokinesis and cardiac function. Conversely, cardiac specific overexpression of LncBAR restores cardiomyocyte proliferation and enhances cardiac regeneration, especially in adult myocardial infarction model. Mechanistically, LncBAR interacts with Brg1, stabilizing BRG1 protein level and activating cell cycle progression to drive cardiomyocytes proliferation. Collectively, our study identified LncBAR as a crucial regulator for heart regeneration, highlighting the LncBAR-BRG1 axis as a promising therapeutic strategy for cardiac repair.

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Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction

Project description:Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction

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USP25 Ameliorates Pathological Cardiac Hypertrophy by Stabilizing SERCA2a in Cardiomyocytes

Project description:USP25 Ameliorates Pathological Cardiac Hypertrophy by Stabilizing SERCA2a in Cardiomyocytes

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Egr1 regulates regenerative senescence and cardiac repair

Project description:Egr1 regulates regenerative senescence and cardiac repair

| PRJNA1065443 | ENA

Chemoprevention with COX2 and EGFR inhibition in FAP patients: mRNA signatures of duodenal neoplasia

Project description:RNA sequencing of duodenal polyps in FAP patients treated with plabebo or the drug combination, erlotinib + sulindac

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EP2 receptor modulates macrophage activity for cardiac repair

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Pouch transcriptional differences between UC and FAP indicate altered immune response.

Project description:A total proctocolectomy with ileal pouch-anal anastomosis (IPAA) is considered the surgery of choice for definitive management of familial adenomatous polyposis (FAP) and selected patients with ulcerative colitis (UC). However, this surgical treatment often associates with a long-term complication, pouchitis, which occurs mostly in UC patients. To better define the molecular background of pouchitis, the microarray-based survey was performed using pouch mucosal samples collected from 28 and 8 patients operated for UC and FAP, respectively. A number of 4771 genes was significantly differentiating uninflamed from inflamed mucosal samples, and their functional features were represented mostly by alerted metabolic and cell proliferation pathways. In contrast, functional analyses of aberrantly expressed probe sets between UC and FAP samples, irrespectively of mucosal inflammation status, revealed multiple pathways and terms which were linked to changes in immune response. Noteworthy, the comparison of uninflamed UC and FAP samples distinguished a set of 26 altered mRNAs including inflammation-related transcript encoding a Charcot-Leyden crystal (CLC) protein. The most discrete changes in gene expression profiles differentiating uninflamed UC and FAP mucosal samples were attributed to a Gene Ontology category innate immune response. Our study confirmed alterations of the immune responses as dominant in UC pouchitis which were earlier found in the studies using analyses of singular molecular elements. This observation may be important when managing IPAA patients. Each sample represents three biopsies taken from single patient, from the same areas of the lower part of the pouch mucosa (above the rectal cuff) during endoscopic examination. 28 patients underwent surgery for UC and 8 patients for FAP.

2014-05-01 | E-GEOD-50788 | biostudies-arrayexpress

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