Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 12

Similar Datasets

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

| PRJNA1090894 | ENA

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

Innate mesenchymal TLR4/MyD88 signals promote spontaneous intestinal tumorigenesis

Project description:Innate mesenchymal TLR4/MyD88 signals promote spontaneous intestinal tumorigenesis

| PRJNA488809 | ENA

Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88

Project description:Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.

2018-10-05 | GSE82200 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data