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Fat graft survival requires metabolic reprogramming towards glycolytic pathway

ABSTRACT: Fat graft survival requires metabolic reprogramming towards glycolytic pathway

PROVIDER: PRJNA841563 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19355935_1.fastq.gz	Fastqsanger.gz
	SRR19355935_2.fastq.gz	Fastqsanger.gz
	SRR19355936_1.fastq.gz	Fastqsanger.gz
	SRR19355936_2.fastq.gz	Fastqsanger.gz
	SRR19355937_1.fastq.gz	Fastqsanger.gz

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Fat graft survival requires metabolic reprogramming towards glycolytic pathway

Project description:Background: The mechanisms underlying fat graft survival are poorly understood. Here, we performed unbiased transcriptomics analysis of mouse fat graft model to find out the molecular mechanism of free fat graft survival. Methods: We conducted RNA-sequencing (RNA-seq) analysis of mouse free subcutaneous fat graft model at day 3 and 7 following grafting (n=5). High-throughput sequencing was performed as paired-end using NovaSeq6000 (Illumina, CA, USA). The calculated transcripts per million (TPM) values were processed for principal component analysis (PCA), unsupervised hierarchically clustered heat map generation, and Gene set enrichment analysis. Results: PCA and heat map data revealed global differences in the transcriptome of grafted fat when compared with non-graft control. The top meaningful up-regulated gene sets in the grafted fat were related to epithelial mesenchymal transition and hypoxia by day 3, and angiogenesis by day 7. Mechanistically, the glycolysis pathway was commonly upregulated in the grafted fat at day 3 (FDR q=0.012) and day 7 (FDR q=0.084). In subsequent experiments, pharmacological inhibition of glycolytic pathway in the grafted fat with 2-Deoxy-D-glucose (2-DG) significantly suppressed fat graft retention rates, both grossly and microscopically (n=5). Conclusions: Global transcriptome analysis and pharmacologic inhibition study revealed that free adipose tissue grafts undergo metabolic reprogramming towards glycolytic pathway. Whether targeting the pathway wound enhance graft survival rate remains to be investigated.

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Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

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Glutathione supplementation improves fat graft survival by inhibiting ferroptosis via the SLC7A11/GPX4 axis

Project description:Background: Autologous fat grafting is hampered by unpredictable graft survival, which is potentially regulated by ferroptosis. Glutathione (GSH), a powerful antioxidant used in tissue preservation, has ferroptosis-regulating activity; however, its effects on fat grafts are unclear. This study investigated the effects and mechanisms of GSH in fat graft survival. Methods: Human lipoaspirates were transplanted subcutaneously into the backs of normal saline-treated (control) or GSH-treated nude mice. Graft survival was evaluated by magnetic resonance imaging and histology. RNA sequencing was performed to identify differentially expressed genes and enriched pathways. GSH activity was evaluated in vitro using an oxygen and glucose deprivation (OGD) model of adipose-derived stem cells. Results: Compared with control group, GSH induced better outcomes, including superior graft retention, appearance, and histological structures. RNA sequencing suggested enhanced negative regulation of ferroptosis in the GSH-treated grafts, which showed reduced lipid peroxides, better mitochondrial ultrastructure, and SLC7A11/GPX4 axis activation. In vitro, OGD-induced ferroptosis was ameliorated by GSH, which restored cell proliferation, reduced oxidative stress, and upregulated ferroptosis defense factors. Conclusions: Our study confirms that ferroptosis participates in regulating fat graft survival and that GSH exerts a protective effect by inhibiting ferroptosis. GSH-assisted lipotransfer is a promising therapeutic strategy for future clinical application.

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Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

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Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [II]

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Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [I]

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation [I]

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Enhancing High-Quality Fat Survival: A Novel Strategy Using Cell Free Fat Extract

Project description:High-quality fat (HQF) contains a higher proportion of stromal vascular fraction, adipose-derived stem cells, and extracellular matrix components, surpassing the effectiveness of the traditional Coleman fat grafting method and improving volumetric filling. However, this high-quality fat strategy inevitably leads to a significant amount of unused fat being wasted. CEFFE, a cell-free extract derived from autologous fat tissue, is enriched with bioactive molecules. In this study, we further process the remaining fat from preparing HQF into CEFFE to promote the survival of transplanted fat. Our study introduces CEFFE, from the remaining fat from preparing HQF, as a promising adjunct to HQF grafting, showcasing notable enhancements in graft survival, adipose tissue integrity, and angiogenesis. The observed positive effects on ADSCs, including augmented stemness and adipogenic differentiation potential, further contribute to the overall improvement in fat graft outcomes. While these findings present a novel strategy for addressing the limitations of traditional fat grafting, additional research and clinical studies are imperative to validate the long-term efficacy, safety, and broader applicability of CEFFE in enhancing fat graft survival and promoting tissue regeneration.

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