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Intrinsic cardiac adrenergic (ICA) cells contribute to LPS-induced myocardial dysfunction

ABSTRACT: Intrinsic cardiac adrenergic (ICA) cells contribute to LPS-induced myocardial dysfunction

PROVIDER: PRJNA785267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17085671_1.fastq.gz	Fastqsanger.gz
	SRR17085671_2.fastq.gz	Fastqsanger.gz
	SRR17085672_1.fastq.gz	Fastqsanger.gz
	SRR17085672_2.fastq.gz	Fastqsanger.gz
	SRR17085673_1.fastq.gz	Fastqsanger.gz

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Intrinsic cardiac adrenergic (ICA) cells contribute to LPS-induced myocardial dysfunction

Project description:The role of ICA cells in septic cardiomyopathy is unknown. Here we show that norepinephrine (NE) secretion from ICA cells is increased through activation of Toll-like receptor 4 (TLR4) to aggravate myocardial TNF-α production and dysfunction by lipopolysaccharide (LPS). In ICA cells, LPS activated TLR4-MyD88/TRIF-AP-1 signaling that promoted NE biosynthesis through expression of tyrosine hydroxylase, but did not trigger TNF-α production due to impairment of p65 translocation. Our findings suggest that ICA cells may be a potential therapeutic target for septic cardiomyopathy.

2022-02-02 | GSE189964 | GEO

Alpha-1 adrenergic signaling drives cardiac regeneration through activation of extracellular matrix remodeling transcriptional program in macrophages

Project description:Autonomic drive plays a pivotal role in cardiac regeneration. Sympathetic or cholinergic denervation impairs myocardial regrowth in neonatal mouse and zebrafish hearts. Here, we uncovered the mechanistic underpinning of adrenergic signaling in regenerative repair of the heart to be critically dependent on immunomodulation. Through pharmacological and genetic manipulations, we identified adrenergic receptor alpha-1 as a key regulator of macrophage phenotypic diversification following myocardial infarction in zebrafish. Single-cell transcriptomics revealed that the receptor signals activation of an ‘extracellular matrix remodeling’ transcriptional program characterized by upregulation of matrix proteins and matrix-modifying enzymes in a macrophage subset. Functionally, adrenergic receptor alpha-1-activated macrophages regulate fibrotic response of the heart by mediating collagenous extracellular matrix turnover and myofibroblast activation, allowing vascularization and cardiomyocyte cell cycle entry at the infarcted lesion. These findings not only unravel the mechanism of adrenergic signaling in macrophage phenotypic and functional determination, but also highlight the potential of neural modulation for regulation of fibrosis and coordination of myocardial regenerative response.

2023-09-21 | GSE205103 | GEO

Pre-existent adult sox10+ cardiomyocytes contribute to myocardial regeneration in the zebrafish

Project description:Pre-existent adult sox10+ cardiomyocytes contribute to myocardial regeneration in the zebrafish

| PRJNA551951 | ENA

Cardiac pericytes contribute to myofibroblast expansion and vascular maturation following myocardial infarction

Project description:Cardiac pericytes contribute to myofibroblast expansion and vascular maturation following myocardial infarction

| PRJNA922047 | ENA

Extrinsic inflammatory, but not intrinsic oligodendroglial factors contribute to oligodendroglial differentiation block in multiple sclerosis

Project description:Multiple sclerosis (MS) is the most frequent demyelinating disease and despite significant advances in the immunotherapy, disease progression still cannot be prevented. Promotion of remyelination, an endogenous repair process, represents a promising new treatment approach. However, spontaneous remyelination frequently fails in MS lesions due to an impaired differentiation of progenitor cells into mature, myelinating oligodendrocytes. Intrinsic oligodendroglial and extrinsic inflammatory factors may contribute to this differentiation block. Therefore, we compared induced pluripotent stem cell (iPSC)-derived oligodendrocytes (hiOL) from MS patients and healthy controls as well as their response to extrinsic factors. While functional capabilities or proteome compostion of both cell types were virtually indistinguishable, we discovered that Interferon-gamma (IFNÎ³) producing immune cells significantly impaired oligodendroglial differentiation and observed no differences in the functional capabilities or the proteome. In summary, these data indicate that the oligodendroglial differentiation block is not due to intrinsic oligodendroglial factors, but rather caused by the inflammatory environment present in MS lesions. These findings may contribute to the development of remyelination promoting strategies in MS.

2020-09-04 | PXD016043 | Pride

A novel class of tRNA-derived small non-coding RNAs in response to myocardial hypertrophy and contribute to intergenerational inheritance

Project description:tRNA-derived fragments (tRFs) have served as new class of non-coding RNA and played important role in regulating cellular RNA processing and protein translation, which was also proved have function on the intergenerational effects of paternal disease. However, there was no study reported the influence of tRFs on myocardial hypertrophy. In the current study, we explore the hypothesis that tRFs in response to myocardial hypertrophy and contribute to intergenerational inheritance.We used isoproterenol induced myocardial hypertrophy rat model. Small RNA (< 40 nt) tanscriptome sequencing was used to select differential expressed tRFs. We over-expressed the highest foldchange tRFs on H9c2 cell to check its function in enlarging cardiocytes surface area. We also compared the tRFs expression pattern in F0 sperm and F1 offspring heart between myocardial hypertrophy (Hyp) and control group (Con), as well as evaluated the phynotype of myocardial hypertrophy in F1 offspring. ISO successfully induced a typical cardiac hypertrophy model in our study. Small RNA-seq revealed tRFs were extremely enriched (84%) in Hyp heart. Overexpression tRFs1 and tRFs2 would both enlarge the surface area of cardiac cell and increase hypertrophic markers (ANF, BNP, and β-MHC) expression. tRFs1, tRFs2, tRFs3 and tRFs4 were also significantly high expressed in Hyp F0 sperm and in Hyp F1 offspring heart, but no function of tRFs7, tRFs9 and tRFs10. Compared to Con F1 offspring, Hyp F1 offspring had high expression levels of β-MHC and ANP genes, and increased fibrosis levles and apoptotic cell in heart.We demonstrate that tRFs are involved in regulating the response of myocardial hypertrophy, it might serve as novel epigenetic factor and contribute to intergenerational inheritance of cardiac hypertrophy.

2017-11-04 | GSE106511 | GEO

Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [scRNA-seq]

Project description:Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [scRNA-seq]

| PRJNA1098025 | ENA

Bacterial Adrenergic signaling

Project description:The ability to respond to stress is at the core of an organism’s survival. The hormones epinephrine and norepinephrine play a central role in stress responses in mammals, which require the synchronized interaction of the whole neuroendocrine system. Bacteria also sense and respond to epinephrine and norepinephrine as a means to gauge the metabolic and immune state of the host. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs), bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to multiple signals and transfer this phosphate to response regulators (RRs). Two bacterial adrenergic receptors have been identified in EHEC, QseC and QseE, with QseE being downstream of QseC in this signaling cascade. We mapped the QseC signaling cascade in the deadly pathogen enterohemorrhagic E. coli (EHEC), which exploits this signaling system to promote disease. Through QseC, EHEC activates expression of metabolic, virulence and stress response genes, synchronizing the cell response to these stress hormones. Coordination of these responses is achieved by QseC phosphorylating three of the thirty two EHEC RRs. The QseB RR, which is QseC’s cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is phosphorylated by the QseE adrenergic sensor, coordinates expression of virulence genes involved in formation of lesions in the intestinal epithelia by EHEC, and the bacterial SOS stress response. The third RR, KdpE, controls potassium uptake, osmolarity response, and also the formation of lesions in the intestine. Adrenergic regulation of bacterial gene expression shares several parallels with mammalian adrenergic signaling having profound effects in the whole organism. Understanding adrenergic regulation of a bacterial cell is a powerful approach to study the underlying mechanisms of stress and cellular survival.

2009-09-15 | GSE15050 | GEO

Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [bulk RNA-seq]

Project description:Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [bulk RNA-seq]

| PRJNA1098021 | ENA

Gene expression signatures of CD11b+ cells in mice after myocardial infarction

Project description:To further search for potential gene targets which are involved in the pathological process of myocardial infarction, we have employed whole genome microarray expression profiling as a discovery platform to identify the expression of STAT6, β1-adrenergic receptors and inflammatory cytokines. The CD11b+ cells were isolated from spleen and bone marrow of mice by magnetic beads, and the experimental mice were divided into four time points (control, MI 1week, MI 2 weeks, and MI 4 weeks). We found the β1-AR related sympathetic signal, the STAT6 signal and inflammatory cytokines (IL-1α, IL-18 and TGF-β) are involved in the activation of CD11b+ immune cells and cardiac fibrogenesis after myocardial infarction.

2020-11-16 | GSE154733 | GEO

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