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The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration

ABSTRACT: The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration

PROVIDER: PRJNA1091566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28435452_1.fastq.gz	Fastqsanger.gz
	SRR28435452_2.fastq.gz	Fastqsanger.gz
	SRR28435453_1.fastq.gz	Fastqsanger.gz
	SRR28435453_2.fastq.gz	Fastqsanger.gz
	SRR28435454_1.fastq.gz	Fastqsanger.gz

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The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration

Project description:The innate immune response is triggered rapidly after injury and its spatiotemporal dynamics are critical for regeneration, but many questions remain about its exact role. Here we show that MyD88, a key component of the innate immune response, controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88-/- ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen-rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88-/- endocardium and increased myofibroblasts and scarring. Notably, endothelial-specific overexpression of myd88 reverses these neutrophil, fibrotic, and scarring phenotypes. Mechanistically, we identify the endocardial-derived chemokine gene cxcl18b as a target of the MyD88-signaling pathway, and using loss- and gain-of-function tools show that it controls neutrophil recruitment. Altogether, these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration.

2024-07-29 | GSE262351 | GEO

The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration

Project description:This SuperSeries is composed of the SubSeries listed below. The innate immune response is triggered rapidly after injury and its spatiotemporal dynamics are critical for regeneration, but many questions remain about its exact role. Here we show that MyD88, a key component of the innate immune response, controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88-/- ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen-rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88-/- endocardium and increased myofibroblasts and scarring. Notably, endothelial-specific overexpression of myd88 reverses these neutrophil, fibrotic, and scarring phenotypes. Mechanistically, we identify the endocardial-derived chemokine gene cxcl18b as a target of the MyD88-signaling pathway, and using loss- and gain-of-function tools show that it controls neutrophil recruitment. Altogether, these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration.

2024-07-29 | GSE262248 | GEO

The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration (dst169)

Project description:The innate immune system is triggered rapidly after injury and its spatiotemporal dynamics are critical for successful regeneration. MyD88 is a key component of the innate immune response; however, its role during regeneration remains unclear. Here we show that MyD88 controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. Our data reveal a significant reduction in pro-inflammatory neutrophil and macrophage populations, as well as the expansion of a collagen-rich endocardial population in cryoinjured myd88-/- ventricles. Consistent with these findings, we observed increased myofibroblasts, fibrin abundance, and scarring in myd88-/- ventricles. Transcriptomic analyses of endocardial cells and immunostaining experiments reveal compromised PI3K/AKT pathway activation in the myd88-/- endocardium. Moreover, loss of MyD88 impairs cardiomyocyte proliferation and protrusive activity towards the injured area. Notably, endothelial-specific overexpression of myd88 reverses the neutrophil, fibrotic, and scarring phenotypes in cryoinjured myd88-/- ventricles. Mechanistically, we identify the endocardial-derived chemokine gene cxcl18b as a transcriptional target of the MyD88-signaling axis and using loss- and gain-of-function tools show that it controls neutrophil recruitment. Altogether, these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis, thereby emphasizing the strong impact of the innate immune response during tissue regeneration.

2024-07-29 | GSE262247 | GEO

The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration

Project description:The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration

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The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration (dst139)

2024-07-29 | GSE262169 | GEO

The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration (dst139)

Project description:The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration (dst139)

| PRJNA1090509 | ENA

The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration (dst169)

Project description:The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration (dst169)

| PRJNA1090898 | ENA

The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration.

Project description:The innate immune response is triggered rapidly after injury and its spatiotemporal dynamics are critical for regeneration; however, many questions remain about its exact role. Here we show that MyD88, a key component of the innate immune response, controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88-/- ventricles a significant reduction in neutrophil and macrophage numbers and the expansion of a collagen-rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88-/- endocardium and increased myofibroblasts and scarring. Notably, endothelial-specific overexpression of myd88 reverses these neutrophil, fibrotic and scarring phenotypes. Mechanistically, we identify the endocardial-derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway, and using loss-of-function and gain-of-function tools, we show that it controls neutrophil recruitment. Altogether, these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration.

| S-EPMC11399109 | biostudies-literature

Myd88

Project description:Rattus norvegicus Myd88, MYD88, innate immune signal transduction adaptor [Source:RGD Symbol;Acc:735043], is differentially expressed in 31 experiment(s);

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Myd88

Project description:Rattus norvegicus Myd88, MYD88, innate immune signal transduction adaptor [Source:RGD Symbol;Acc:735043], is expressed in 7 baseline experiment(s);

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