Abstract
Autologous fat grafting is a gold standard therapy for soft tissue defects, but is hampered by unpredictable postoperative outcomes. Fat graft enrichment with adipose-derived stromal cell (ASCs) was recently reported to enhance graft survival. Platelet-rich plasma (PRP) has also emerged as a biologic scaffold that promotes fat graft viability. Combined ASC/PRP fat grafting enrichment is thus a promising new regenerative medicine approach. The effects of PRP on ASC proliferation are well documented, but the impact of PRP on ASC differentiation has yet to be investigated in depth to further elucidate the PRP clinical effects. Here we analyzed the human ASC fate upon PRP treatment. PRP was found to sharply reduce the potential of ASCs to undergo differentiation into adipocytes. Interestingly, the PRP anti-adipogenic effect was accompanied by the generation of myofibroblast-like cells. Among the various factors released from PRP, TGFβ pathway activators played a critical role in both the anti-adipogenic and pro-myofibroblastic PRP effects. Overall, these data suggest that PRP participates in maintaining a pool of ASCs and in the repair process by promoting ASC differentiation into myofibroblast-like cells. TGFβ may provide an important target pathway to improve PRP clinical outcomes.
Highlights
Autologous fat grafting is a gold standard therapy for soft tissue defects, correction or augmentation in reconstructive and plastic surgery
We show that the six individually tested Platelet-rich plasma (PRP) dramatically inhibited knee-adipose-derived stromal/stem cells (ASCs) adipocyte formation when used at 20%, as revealed by the lower number of adipocytes and lipid contents quantified in the PRP-treated cultures (Fig. S2)
The effect was confirmed at the molecular level, as shown by the lower expression of adipogenic genes such as PPARγ, AdipoQ and FABP4 in PRP-treated cells (Fig. 1B)
Summary
Autologous fat grafting is a gold standard therapy for soft tissue defects, correction or augmentation in reconstructive and plastic surgery. PRP releases factors from members of the transforming growth factor-β (TGF β) family that were shown to be potent anti-adipogenic factors and key mediators in the conversion of human ASCs into myofibroblast-like cells[6, 7]. As excessive collagen deposition is associated with fibrotic lesions, we considered it essential to study the TGFβ pathway with regard to PRP effects on ASC adipogenic and myofibroblastic differentiation.
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