The effects of Platelet-rich plasma on adipogenesis of FAPs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE284069 | GEO | 2025/11/01
REPOSITORIES: GEO
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Project description:Platelet-rich plasma (PRP) is used to treat musculoskeletal diseases, such as rotator cuff tears, and has been proven to attenuate fatty infiltration in muscle injury; however, the effective components are still unclear. Furthermore, PRP is currently strictly used by donors in themselves, and it is unknown whether and how the heterogeneity of donors, especially aging, would change the composition of PRP and impact the therapeutic effects. In this study, we found that young donor-derived exosomes, but not those from old people, were critical components in PRP that regulate fatty infiltration in muscle injury by directly inhibiting adipogenesis of muscle-resident FAPs. The characteristics of young donor-derived PRP exosomes were quite different from those of old donor-derived PRP exosomes. Mechanistically, we demonstrated that two components of miRNA cargo, hsa-let-7f-5p and hsa-miR-16-5p, played an essential role in regulating adipogenesis of FAPs and fatty infiltration by targeting TGFBR3.
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Project description:Chronic rotator cuff injuries can lead to a degenerative microenvironment that favors chronic inflammation, fibrosis, and fatty infiltration. Recovery of muscle structure and function will ultimately require a complex network of muscle resident cells, including satellite cells, fibro-adipogenic progenitors (FAPs), and immune cells. Recent work suggests that signaling from adipose tissue and progenitors could modulate regeneration and recovery of function, particularly pro-myogenic signaling from brown or beige adipose (BAT). In this study, we sought to identify cellular targets of BAT signaling during muscle regeneration using a rotator cuff BAT transplantation mouse model. Cardiotoxin injured supraspinatus muscle had improved mass at 7 day post-surgery (dps) when transplanted with exogeneous BAT. Transcriptional analysis revealed transplanted BAT modulates FAP signaling early in regeneration likely via crosstalk with immune cells.
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Project description:Myosteatosis is the pathological accumulation of lipid that occurs in conjunction with atrophy and fibrosis following skeletal muscle injury or disease. Little is known about the mechanisms by which lipid accumulates in myosteatosis, but many studies have demonstrated the degree of lipid infiltration negatively correlates with muscle function and regeneration. Our goal was to identify biochemical pathways that lead to muscle dysfunction and lipid accumulation in injured rotator cuff muscles, a model that demonstrates severe myosteatosis. Adult rats were subjected to a massive tear to the rotator cuff musculature. After a period of either 0 (healthy control), 10, 30, or 60 days, muscles were prepared for RNA sequencing, shotgun lipidomics, metabolomics, biochemical measures, electron microscopy, and muscle fiber contractility. Following rotator cuff injury, there was a decrease in muscle fiber specific force production that was lowest at 30d. There was a dramatic time dependent increase in triacylglyceride content. Interestingly, genes related to not only triacylglyceride synthesis, but also lipid oxidation were largely downregulated over time. Using bioinformatics techniques, we identified that biochemical pathways related to mitochondrial dysfunction and reactive oxygen species were considerably increased in muscles with myosteatosis. Long chain acyl-carnitines and L-carnitine, precursors to beta-oxidation, were depleted following rotator cuff tear. Electron micrographs showed injured muscles displayed large lipid droplets within mitochondria at early time points, and an accumulation of peripheral segment mitochondria at all time points. Several markers of oxidative stress were elevated following rotator cuff tear. The results from this study suggest that the accumulation of lipid in myosteatosis is not a result of canonical lipid synthesis, but occurs due to decreased lipid oxidation in mitochondria. A failure in lipid utilization by mitochondria would ultimately cause an accumulation of lipid even in the absence of increased synthesis. Further study will identify whether this process is required for the onset of myosteatosis.
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