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Neutrophils direct preexisting matrix in to initiate repair of damaged organs

ABSTRACT: Neutrophils direct preexisting matrix in to initiate repair of damaged organs

PROVIDER: PRJNA817084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18356109_1.fastq.gz	Fastqsanger.gz
	SRR18356109_2.fastq.gz	Fastqsanger.gz
	SRR18356110_1.fastq.gz	Fastqsanger.gz
	SRR18356110_2.fastq.gz	Fastqsanger.gz
	SRR18356111_1.fastq.gz	Fastqsanger.gz

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Neutrophils direct preexisting matrix in to initiate repair of damaged organs

Project description:Internal organs heal injuries with new connective tissue. However the cellular and molecular events, and the sources of this tissue, remain obscure. Here we tagged extracellular matrix around the mesothelium lining various mouse tissues: peritoneum, liver, and cecum, and applied various injury models. We discovered that preexisting matrix is transferred across organs into wounds. Using proteomics, genetic lineage-tracing and by selectively injuring juxtaposed organs, we demonstrate that the matrix tissue of origin likely dictates the final healing outcome: whether scarring or regeneration. Through single-cell RNA sequencing and genetic and chemical screens, we demonstrate that preexisting matrix is transferred by neutrophils in a heat shock factor, integrin AM/B2, kindlin3, cascade and pharmacologic inhibition of this axis prevented matrix transfer and peritoneal adhesions. Matrix transfer is thus an early event of wound repair that creates a therapeutic space to dampen scaring across a range of human conditions.

2022-03-20 | GSE198828 | GEO

Neutrophils direct preexisting matrix to initiate repair in damaged tissues.

Project description:Internal organs heal injuries with new connective tissue, but the cellular and molecular events of this process remain obscure. By tagging extracellular matrix around the mesothelium lining in mouse peritoneum, liver and cecum, here we show that preexisting matrix was transferred across organs into wounds in various injury models. Using proteomics, genetic lineage-tracing and selective injury in juxtaposed organs, we found that the tissue of origin for the transferred matrix likely dictated the scarring or regeneration of the healing tissue. Single-cell RNA sequencing and genetic and chemical screens indicated that the preexisting matrix was transferred by neutrophils dependent on the HSF-integrin AM/B2-kindlin3 cascade. Pharmacologic inhibition of this axis prevented matrix transfer and the formation of peritoneal adhesions. Matrix transfer was thus an early event of wound repair and provides a therapeutic window to dampen scaring across a range of conditions.

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The role of damaged mitochondrial DNA in Parkinson Disease

Project description:Parkinson disease (PD) is a neurodegenerative disease believed to initiate in the brainstem and then spread throughout the brain. The mechanism by which this occurs is not yet fully understood, but here we show that damaged mitochondrial DNA (mtDNA) plays an important role in this process, which can be initiated by dysregulation of the IFNb/IFNAR signalling pathway. We report that lack of neuronal IFNb/IFNAR, which is associated to the development of PD, causes oxidization, mutation, and deletion in mtDNA. Damaged mtDNA is subsequently extruded extracellularly and can induce PD symptoms like motor and cognitive impairments in healthy mouse brains. It even leads to neurodegeneration in brain regions far from the injection site, suggesting that damaged mtDNA triggers the propagation of PD hallmarks through the brain. We further show that the mechanism by which damaged mtDNA causes pathology in healthy neurons is independent of cGAS and IFNb/IFNAR, but it is mediated by activation of dual Toll-like receptor (TLR)4/9 pathways. Through a proteomic analysis of extracellular vesicles containing the damaged mtDNA, we identified the TLR4 activator Ribosomal Protein S3 (Rps3) and established that Rps3 is a key effector protein involved in damaged mtDNA extrusion and recognition. Collectively, these results reveal a new molecular pathway by which damaged mtDNA can initiate and propagate Parkinson's Disease, paving the way for potential new therapies or disease monitoring.

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p63+/Krt5+ Distal Airway Stem Cells are Essential for Lung Regeneration (transplanted and damaged)

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