Lipid metabolism adaptations are reduced in human compared to murine Schwann cells following injury.
Sofia Meyer Zu ReckendorfChristine BrandMaria T PedroJutta HeglerCorinna S SchillingRaissa LernerLaura BindilaGregor AntoniadisBernd KnöllPublished in: Nature communications (2020)
Mammals differ in their regeneration potential after traumatic injury, which might be caused by species-specific regeneration programs. Here, we compared murine and human Schwann cell (SC) response to injury and developed an ex vivo injury model employing surgery-derived human sural nerves. Transcriptomic and lipid metabolism analysis of murine SCs following injury of sural nerves revealed down-regulation of lipogenic genes and regulator of lipid metabolism, including Pparg (peroxisome proliferator-activated receptor gamma) and S1P (sphingosine-1-phosphate). Human SCs failed to induce similar adaptations following ex vivo nerve injury. Pharmacological PPARg and S1P stimulation in mice resulted in up-regulation of lipid gene expression, suggesting a role in SCs switching towards a myelinating state. Altogether, our results suggest that murine SC switching towards a repair state is accompanied by transcriptome and lipidome adaptations, which are reduced in humans.
Keyphrases
- endothelial cells
- gene expression
- induced pluripotent stem cells
- stem cells
- single cell
- pluripotent stem cells
- minimally invasive
- dna methylation
- genome wide
- fatty acid
- high intensity
- metabolic syndrome
- skeletal muscle
- mesenchymal stem cells
- transcription factor
- adipose tissue
- climate change
- coronary artery disease
- genome wide identification
- percutaneous coronary intervention