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Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis

ABSTRACT: Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis

PROVIDER: PRJNA916716 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22926639.fastq.gz	Fastqsanger.gz
	SRR22926640.fastq.gz	Fastqsanger.gz
	SRR22926641.fastq.gz	Fastqsanger.gz
	SRR22926642.fastq.gz	Fastqsanger.gz
	SRR22926643.fastq.gz	Fastqsanger.gz

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Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis

Project description:We developed an on-slide decellularization approach to generate acellular extracellular matrix (ECM) scaffolds that can be repopulated with various cell types to interrogate cell-ECM interactions. Using this platform, we investigated whether fibrotic ECM scarring affected human skeletal muscle progenitor cell (SMPC) functions that are essential for myoregeneration. SMPCs exhibited robust adhesion, motility, and differentiation on healthy muscle-derived myoscaffolds. All SPMC interactions with fibrotic myoscaffolds from dystrophic muscle were severely blunted including reduced motility rate and migration. Furthermore, SMPCs were unable to remodel laminin dense fibrotic scars within diseased myoscaffolds. Proteomics and structural analysis revealed that excessive collagen deposition alone is not pathological, and can be compensatory, as revealed by overexpression of sarcospan and its associated ECM receptors in dystrophic muscle. Our in vivo data also supported that ECM remodeling is important for SMPC engraftment and that fibrotic scars may represent one barrier to efficient cell therapy.

2022-12-29 | GSE221912 | GEO

Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis.

Project description:We developed an on-slide decellularization approach to generate acellular extracellular matrix (ECM) myoscaffolds that can be repopulated with various cell types to interrogate cell-ECM interactions. Using this platform, we investigated whether fibrotic ECM scarring affected human skeletal muscle progenitor cell (SMPC) functions that are essential for myoregeneration. SMPCs exhibited robust adhesion, motility, and differentiation on healthy muscle-derived myoscaffolds. All SPMC interactions with fibrotic myoscaffolds from dystrophic muscle were severely blunted including reduced motility rate and migration. Furthermore, SMPCs were unable to remodel laminin dense fibrotic scars within diseased myoscaffolds. Proteomics and structural analysis revealed that excessive collagen deposition alone is not pathological, and can be compensatory, as revealed by overexpression of sarcospan and its associated ECM receptors in dystrophic muscle. Our in vivo data also supported that ECM remodeling is important for SMPC engraftment and that fibrotic scars may represent one barrier to efficient cell therapy.

| S-EPMC10017766 | biostudies-literature

Human Scarring Project

Project description:Full thickness and deep partial thickness burn injuries heal by scarring. There are several mechanisms thought to be essential for the development of burn scars, but a challenge to studying the skin response to burn injury is that there are few animal models of burn scarring that are either clinically similar to human burn scars or are practical for most investigators to use. The purpose of this study was to examine the changes in RNA expression in human skin to burn injury. This was done by comparing pre-injury tissue from otherwise healthy adults undergoing aesthetic scarification created by branding with a hot metal object to serial samples of untreated wounds in the same subjects.

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Project description:Comparison of laminin binding and laminin non-binding germ cells Keywords: other

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Transcription profiling of laminin binding and laminin non-binding germ cells to define the spermatogonial stem cells.

Project description:Comparison of laminin binding and laminin non-binding germ cells.

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Cross-linking of mouse laminin 111

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Mechanotransduction inhibition prevents scarring and yields regeneration in a large animal model

Project description:Inhibiting mechanotransduction (via Yes-associated protein [YAP] inhibition) in mouse wounds yields wound regeneration without scarring. However, rodents are loose-skinned and fail to recapitulate key aspects of human wound repair. We thus sought to elucidate the effects of YAP inhibition in red Duroc pig wounds, the most human-like model of scarring. We show that a single treatment with the YAP inhibitor verteporfin, immediately following wounding, is sufficient to prevent scarring and drive wound regeneration in pigs. By performing scRNA-seq for the first time on porcine wounds in conjunction with spatial protein analysis, we reveal perturbations in fibroblast subpopulation profiles with verteporfin treatment and the presence of putative pro-regenerative and pro-fibrotic fibroblast subsets enriched in regenerating and scarring pig wounds, respectively. Finally, we validate our findings in a human foreskin xenograft wound model, including scRNA-seq of human wound cells. Collectively, our findings provide critical support for the future translation of local mechanotransduction inhibitors to prevent human skin scarring.

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