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Preprints

The efficacy and mechanism of platelet-rich plasma on the myogenic differentiation process of adipose-derived stem cell: A bioinformatics and experimental study

Wang X, Fei W, Liu M, Shen F, Liu Y, Gu S.
Preprint from
Research Square
25 May 2022
PPR
PPR498522
Abstract

Background:

Platelet-rich plasma (PRP) can effectively treat injury of musculoskeletal system, but there is no consensus on whether it can effectively promote the myogenic differentiation of adipose mesenchymal stem cells. Methods Dataset of PRP in the treatment of musculoskeletal injury was obtained by GEO database and the key pathways of PRP were identified by KEGG enrichment analysis. PPI network was constructed by Cytoscape and core gene was identified by the MOCODE. ADSCs were clutivated in vitro and 5-Aza combined PRP were added. MTT were performed to determine the cell viability. Cell senescence was detected by β-galactosidase. Immunofluorescence staining was used to detect the expression of MHC and MyoD. Core gene expression was detected by RT-PCR. Mito-tracker staining and transmission electron microscope were performed respectively. Results GSE70918 was obtained and 148 differentially expressed genes were obtained. KEGG analysis showed the differential genes were enriched in GPCR-related pathways. CCL2 was set as core gene. MTT showed that PRP significantly increase the viability of ADSCs and the IC50 was 19.4 µmol/L. After the addition of 5-Aza combined with PRP, β-galactosidase showed the number of senescent cells decreased significantly, immunofluorescence staining showed the expression of MHC and MyoD increased significantly, RT-PCR showed the expression of CCL-2 decreased significantl, mito-tracker staining showed the number of mitochondria increased and transmission electron microscopy showed the number of mitophagy increased significantly. Conclusion PRP can effectively protect the viability of ADSCs, promote myogenic differentiation efficiency and promote mitophagy. The above functions may be caused by inhibiting the expression of CCL-2.