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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

Intrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction.

Project description:Intrinsic cardiac adrenergic (ICA) cells regulate both developing and adult cardiac physiological and pathological processes. However, 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. In a co-culture consisting of LPS-treated ICA cells and cardiomyocytes, the upregulation and secretion of NE from ICA cells activated cardiomyocyte β1-adrenergic receptor driving Ca2+/calmodulin-dependent protein kinase II (CaMKII) to crosstalk with NF-κB and mitogen-activated protein kinase pathways. Importantly, blockade of ICA cell-derived NE prevented LPS-induced myocardial dysfunction. Our findings suggest that ICA cells may be a potential therapeutic target for septic cardiomyopathy.

| S-EPMC8789803 | biostudies-literature

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

Leukocyte-intrinsic ER stress responses contribute to chemotherapy-induced peripheral neuropathy.

Project description:Leukocyte-intrinsic ER stress responses contribute to chemotherapy-induced peripheral neuropathy.

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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

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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

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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]

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Involvement of Icaritin in the Regulation of Osteocyte Exosomal MicroRNAs

Project description:In this study, we isolated exosomes from ICA-treated osteocytes and sequenced small RNAs from them and controls with the aim of exploring the regulatory role of ICA on osteocyte exosomal miRNAs, which in turn can contribute to the understanding of the potential molecular mechanisms involved in bone repair by ICA.

2025-02-19 | GSE254351 | GEO

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