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

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

PROVIDER: PRJNA852258 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19805736.fastq.gz	Fastqsanger.gz
	SRR19805737.fastq.gz	Fastqsanger.gz
	SRR19805738.fastq.gz	Fastqsanger.gz
	SRR19805739.fastq.gz	Fastqsanger.gz
	SRR19805740.fastq.gz	Fastqsanger.gz

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

Project description:To explore the impact of targeting IL-10 signaling, tibialis anterior (TA) VML injuries were created and then treated in Sprague Dawley rats using an autologous minced muscle regenerative medicine repair strategy in combination with delayed exogenous IL-10 delivery. We then performed gene expression profiling analysis using data obtained from RNA-seq from rat muscles (n=4 for IL-10 treatment, n=4 for PBS control , and n=4 for uninjured control) at day 14 post injury

2022-06-26 | GSE206823 | GEO

Transcriptomic profile of monocytes/macrophages from mice with bone, muscle, skin or heart injuries that were treated with systemic delivery of Tregs

Project description:Mice with either a cranial bone defect, skin biopsy punch injury, quadriceps volumetric muscle loss defect or myocardial infarction (MI) were treated with Tregs, either via local hydrogel-mediated delivery (for bone, muscle and skin), or with systemic (intravenous) delivery (for heart). Control mice were treated with hydrogel alone (for bone, muscle and skin) or PBS (for heart). On day 4 and 7 post-MI, the injured tissues were harvested and the endogenous monocytes/macrophages were sorted and used for mini-bulk RNA sequencing, to compare the transcriptomic profiles of injured tissue monocytes/macrophages in Treg-treated and untreated mice post-injury.

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

Project description:This study was designed to test the hypothesis that in addition to repairing the architectural and cellular cues via regenerative medicine, the delivery of immune cues (immunotherapy) may be needed to enhance regeneration following volumetric muscle loss (VML) injury. We identified IL-10 signaling as a promising immunotherapeutic target. To explore the impact of targeting IL-10 signaling, tibialis anterior (TA) VML injuries were created and then treated in rats using autologous minced muscle (MM). Animals received either recombinant rat IL-10 or phosphate buffered saline (PBS) controls injections at the site of VML repair beginning 7 days post injury (DPI) and continuing every other day (4 injections total) until 14 DPI. At 56 DPI (study endpoint), significant improvements to TA contractile torque (82% of uninjured values & 170% of PBS values), TA mass, and myofiber size in response to IL-10 treatment were detected. Whole transcriptome analysis at 14 DPI revealed activation of IL-10 signaling, muscle hypertrophy, and lymphocytes signaling pathways. Expression of ST2, a regulatory T (Treg) cell receptor, was dramatically increased at the VML repair site in response to IL-10 treatment when compared to PBS controls. The findings suggest that the positive effect of delayed IL-10 delivery might be due to immuno-suppressive Treg cell recruitment.

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Unwavering Pathobiology of Volumetric Muscle Loss Injury

Project description:Unwavering Pathobiology 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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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.

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Transcriptome profiling of the early response to volumetric muscle loss repair strategies

Project description:Transcriptome profiling of the early response to volumetric muscle loss repair strategies

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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.

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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.

2024-01-18 | GSE215808 | GEO

Spatiotemporal mapping of immune and stem cell dysregulation after volumetric muscle loss

Project description:Volumetric muscle loss (VML) is an acute trauma that results in persistent inflammation, supplantation of muscle tissue with fibrotic scarring, and decreased muscle function. The cell types, nature of cellular communication, and tissue locations that drive the aberrant VML response have remained elusive. Herein, we used spatial transcriptomics on mouse and canine models of VML and observed VML engenders a unique spatial pro-fibrotic pattern driven by crosstalk between fibrotic and inflammatory macrophages and mesenchymal derived cells. The dysregulated response was conserved between murine and canine VML models, albeit with varying kinetics, and impinged on muscle stem cell mediated repair. Targeting this circuit in a murine model resulted in increased regeneration and reductions in inflammation and fibrosis. Collectively, these results enhance our understanding of the cellular crosstalk that drives aberrant regeneration and provides further insight into possible avenues for fibrotic therapy exploration.

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