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Immunoresolving lipid mediators support effective skeletal muscle repair

ABSTRACT: Immunoresolving lipid mediators support effective skeletal muscle repair

PROVIDER: PRJNA611966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11289031.fastq.gz	Fastqsanger.gz
	SRR11289032.fastq.gz	Fastqsanger.gz
	SRR11289033.fastq.gz	Fastqsanger.gz
	SRR11289034.fastq.gz	Fastqsanger.gz
	SRR11289035.fastq.gz	Fastqsanger.gz

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Immunoresolving lipid mediators support effective skeletal muscle repair

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Project description:The development of insulin resistance is strongly associated with accumulation of intracellular lipid in tissues outside of adipose including skeletal muscle, liver and heart. In obese humans, intramyocellular lipid (IMCL) is negatively correlated with whole body insulin sensitivity. The skeletal myocyte imports fatty acids (FA) into the cell from circulating free fatty acids or lipoprotein particles such as VLDL, to support energy production. Once transported into the cell, FAs are oxidized for ATP production, used to build membranes, or stored as triglyceride. However, in the long term, increased delivery of fatty acids can exceed mitochondrial oxidative capacity and set the stage for a vicious cycle of cellular lipotoxicity. We have recently identified a novel small molecule inhibitor of lipid accumulation in skeletal mycytes termed SBI-477. Microarray transcriptomics was performed in primary human skeletal myotubes following oleate loading and treatment with SBI-477. This was also compared to A922500, a diacylglycerol transferase 1 (DGAT1) inhibitor. SBI-477 treatment reversed many of the transcriptomic effects of oleate loading in these cells but also produced a transcriptomic profile distinct from the DGAT1 inhibitor. Microarray expression profiling was performed with total RNA isolated from differentiated primary human skeletal myotubes. These cells were treated with BSA (control for oleate), 100micromolar oleic acid, oleate + 10micromolar SBI-477 and oleate + 1micromolar A922500 for 24 hours. Oleate and test compound were added at the same time to the cells. Two biologic replicates for each condition were included.

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Novel Lipid Signaling Mediators for Mesenchymal Stem Cell Mobilization during Bone Repair.

Project description:IntroductionMesenchymal stem and progenitor cells (MSCs), which normally reside in the bone marrow, are critical to bone health and can be recruited to sites of traumatic bone injury, contributing to new bone formation. The ability to control the trafficking of MSCs provides therapeutic potential for improving traumatic bone healing and therapy for genetic bone diseases such as hypophosphatasia.MethodsIn this study, we explored the sphingosine-1-phosphate (S1P) signaling axis as a means to control the mobilization of MSCs into blood and possibly to recruit MSCs enhancing bone growth.ResultsLoss of S1P receptor 3 (S1PR3) leads to an increase in circulating CD45-/CD29+/CD90+/Sca1 putative mesenchymal progenitor cells, suggesting that blocking S1PR3 may stimulate MSCs to leave the bone marrow. Antagonism of S1PR3 with the small molecule VPC01091 stimulated acute migration of CD45-/CD29+/CD90+/Sca1+ MSCs into the blood as early as 1.5 hours after treatment. VPC01091 administration also increased ectopic bone formation induced by BMP-2 and significantly increased new bone formation in critically sized rat cranial defects, suggesting that mobilized MSCs may home to injuries to contribute to healing. We also explored the possibility of combining S1P manipulation of endogenous host cell occupancy with exogenous MSC transplantation for potential use in combination therapies. Importantly, reducing niche occupancy of host MSCs with VPC01091 does not impede engraftment of exogenous MSCs.ConclusionsOur studies suggest that MSC mobilization through S1PR3 antagonism is a promising strategy for endogenous tissue engineering and improving MSC delivery to treat bone diseases.

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