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Unwavering Pathobiology of Volumetric Muscle Loss Injury

ABSTRACT: Unwavering Pathobiology of Volumetric Muscle Loss Injury

PROVIDER: PRJNA472640 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7207360_1.fastq.gz	Fastqsanger.gz
	SRR7207360_2.fastq.gz	Fastqsanger.gz
	SRR7207361_1.fastq.gz	Fastqsanger.gz
	SRR7207361_2.fastq.gz	Fastqsanger.gz
	SRR7207362_1.fastq.gz	Fastqsanger.gz

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Unwavering Pathobiology of Volumetric Muscle Loss Injury

Project description:Volumetric muscle loss (VML) resulting from extremity trauma presents chronic and persistent functional deficits which ultimately manifest disability. Acellular biological scaffolds, or decellularized extracellular matrices (ECMs), embody an ideal treatment platform due to their current clinical use for soft tissue repair, off-the-shelf availability, and zero autogenous donor tissue burden. ECMs have been reported to promote functional skeletal muscle tissue remodeling in small and large animal models of VML injury, and this conclusion was reached in a recent clinical trial that enrolled 13 patients. However, numerous other pre-clinical reports have not observed ECM-mediated skeletal muscle regeneration. The current study was designed to reconcile these discrepancies. The capacity of ECMs to orchestrate functional muscle tissue remodeling was interrogated in a porcine VML injury model using unbiased assessments of muscle tissue regeneration and functional recovery. Here, we show that VML injury incites an overwhelming inflammatory and fibrotic response that leads to expansive fibrous tissue deposition and chronic functional deficits, which ECM repair does not augment.

2018-05-23 | GSE114798 | GEO

Deconstruction of cellular dynamics after treatment of volumetric muscle loss injury with extracellular matrix

Project description:Volumetric muscle loss (VML) is an acute loss of a critical volume of skeletal muscle that results in inflammation, fibrotic scarring in muscle tissue, and permanent muscle defects. The cellular and molecular processes that underlie fibrosis induced from VML injury need to be evaluated in larger animal models. Therefore, we used a canine model of VML alongisde treatment with an extracellular matrix (ECM) hydrogel. Treatment with the ECM hydrogel improved muscle regenerative responses and decreased proportions and spatial signatures of fibrotic and inflammatory cell populations.

2024-06-01 | GSE266585 | GEO

Multiscale analysis of a regenerative therapy for treatment of volumetric muscle loss injury

Project description:Skeletal muscle possesses a remarkable capacity to regenerate when injured, but when confronted with major traumatic injury resulting in volumetric muscle loss (VML), the regenerative process consistently fails. The loss of muscle tissue and function from VML injury has prompted development of a suite of therapeutic approaches but these strategies have proceeded without a comprehensive understanding of the molecular landscape that drives the injury response. Herein, we administered a VML injury in an established rodent model and monitored the evolution of the healing phenomenology over multiple time points using muscle function testing, histology, and expression profiling by RNA sequencing. The injury response was then compared to a regenerative medicine treatment using orthotopic transplantation of autologous minced muscle grafts (~1 mm3 tissue fragments). A chronic inflammatory and fibrotic response was observed at all time points following VML. These results suggest that the pathological response to VML injury during the acute stage of the healing response overwhelms endogenous and therapeutic regenerative processes. Overall, the data presented delineate key molecular characteristics of the pathobiological response to VML injury that are critical effectors of effective regenerative treatment paradigms.

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Project description:The acute traumatic or surgical loss of skeletal muscle, known as volumetric muscle loss (VML), is a devastating type of injury that results in exacerbated and persistent inflammation followed by fibrosis. The mechanisms that mediate the magnitude and duration of the inflammatory response and ensuing fibrosis after VML remain understudied, and as such, the development of regenerative therapies has been limited. To address this need, we profiled how lipid mediators, which are potent regulators of the immune response after injury, varied with VML injuries that heal or result in fibrosis. We observed that non-healing VML injuries displayed increased pro-inflammatory eicosanoids and a lack of pro-resolving lipid mediators. Treatment of VML with a pro-resolving lipid mediator synthesized from docosahexaenoic acid, called Maresin 1, ameliorated fibrosis through reduction of neutrophils and macrophages and enhanced recovery of muscle strength. These results expand our knowledge of the dysregulated immune response that develops after VML and identify a novel immuno-regenerative therapeutic modality in Maresin 1.

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Multiscale analysis of a regenerative therapy for treatment of volumetric muscle loss injury

Project description:Multiscale analysis of a regenerative therapy for treatment of volumetric muscle loss injury

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Maresin 1 Repletion Improves Muscle Regeneration After Volumetric Muscle Loss

Project description:Maresin 1 Repletion Improves Muscle Regeneration After Volumetric Muscle Loss

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Deconstruction of cellular dynamics after treatment of volumetric muscle loss injury with extracellular matrix

Project description:Deconstruction of cellular dynamics after treatment of volumetric muscle loss injury with extracellular matrix

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Unwavering Pathobiology of Volumetric Muscle Loss Injury.

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Local IL-10 delivery modulates the immune response and enhances repair of volumetric muscle loss muscle injury

Project description:Local IL-10 delivery modulates the immune response and enhances repair of volumetric muscle loss muscle injury

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Single cell deconstruction of murine volumetric muscle loss reveals inflammatory imbalances preventing muscle stem cell mediated regeneration

Project description:Volumetric muscle loss (VML) overwhelms the innate regenerative capacity of mammalian skeletal muscle (SkM), leading to numerous disabilities and reduced quality of life. Immune cells are critical responders to muscle injury and guide tissue resident stem cell and progenitor mediated myogenic repair. However, how immune cell infiltration and inter-cellular communication networks are altered following VML and drive pathological outcomes remains under-explored. Herein, we characterize the cellular and molecular mechanisms of VML injuries that result in fibrotic degeneration or regeneration of SkM. Following degenerative VML injuries, we observe heightened infiltration of a previously uncharacterized population of Natural Killer (NK) cells as well as persistence of neutrophils beyond two weeks post injury. Functional validation of NK cells revealed an antagonistic role on neutrophil accumulation in part via CCR1 mediated chemotaxis. The persistent infiltration of neutrophils in degenerative VML injuries was found to contribute to impairments in muscle stem cell regenerative function, which was also attenuated by transforming growth factor beta 1 (TGFb1). Blocking TGFb signaling antagonized neutrophil accumulation, reduced fibrosis, and improved muscle specific force. Collectively, these results enhance our understanding of immune cell-stem cell crosstalk that drives regenerative dysfunction and provide further insight into possible avenues for fibrotic therapy exploration.

2022-04-04 | GSE163376 | GEO

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