Plastic Surgery Research Council
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PSRC 60th Annual Meeting

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Platelet-rich Plasma Promotes Fat Graft Survival via Stemness and Angiogenesis on Adipose-derived Stem Cells
Han-Tsung Liao, MD, PhD, Kokai Lauren, Ph.D, Kacey G. Marra, Ph.D, J Peter Rubin, M.D..
UPMC, Pittsburgh, PA, USA.

Platelet-rich Plasma Promotes Fat Graft Survival via Stemness and Angiogenesis on Adipose-derived Stem Cells
Han-Tsung Liao1,4,Lauren Kokai1, Kacey G Marra1,2,3 ,J Peter Rubin1,2,3
1. Division of Plastic Surgery, University of Pittsburgh, Pittsburgh, PA, USA
2. Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA
3. McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA
4. Division of trauma plastic surgery, Department of Plastic and Reconstructive Surgery, Craniofacial research center, Chang Gung Memorial Hospital, Chang Gung University, Taiwan, R.O.C.
Abstract:
Purpose:
Platelet-rich plasma (PRP) containing multiple growth factors has been documented to enhance bone regeneration, wound healing and muscle or tendon healing. Recently, platelet-rich plasma (PRP) is reported to promote fat graft survival in both animal and clinical studies. However, the molecular mechanism is still not clear. The aim of this study is to determine the possible mechanism via in-vitro and in-vivo nude mice study.
Materials and Methods:
Human Platelets were purchased from HEMOCARE for the production of PRP. Human adipose-derived stem cells were isolated as per laboratory protocol. The ASCs were cultured under four conditions: 1. Regular DMEM medium, 2. Regular DMEM medium with PRP 3. Adipogenic medium 4. Adipogenic medium with PRP. The cell proliferation was assessed by CYQUANT and the adipogenesis were evaluated by AdipoRed stain and the qPCR of PPAR-gamma and FABP4 gene expression. The mRNA of stemness gene expression of ASCs was compared by qPCR of SOX-2, Nanog and Oct-4 .The angiogenesis of ASCs was evaluated by qPCR of VEGF gene expression and endothelium tube formation assay. The nude mice were implant with fat graft with PRP as experiment and fat graft only as control group. The survival rate was analyzed by volume retention, the histomophometry of mature adipocyte area and vessel density assay by CD31 immunohistochemical stain.
Results:
Proliferation of ASCs was enhanced dramatically both in regular DMEM and adipogenic medium with PRP. The PRP-treated ASCs appeared smaller and more spindle in shape than ASCs in regular medium. The up-regulation of Sox-2, Nanog and Oct-4 further proved the more stemness of PRP-treated ASCs. In contrast, intra-cytoplasmic lipid accumulation was decreased after treatment with PRP. The qPCR also confirmed the down-regulation of adipogenesis on both PPAR-gamma and FABP4 gene expression in PRP-treated cells under adipogenic medium. The up-regulation of VEGF expression and the tube formation assay indicated angiogenesis of PRP-treated cells under regular medium. The in-vivo nude mice showed more fat graft retention in the PRP-treated group than fat graft only group (p<0.05). Histology indicated the greater adipocyte survival and more vessel formation in PRP-treated group.
Conclusion:
Taken together, PRP may promote fat graft survival via proliferation of ASCs and its angiogenic effect. The angiogenic effect of PRP itself and PRP-treated ASCs will enhance the vascular supply to maintain the adipocyte survival within fat graft. Furthermore, the stemness effect of PRP increases the renewal and differentiation capabilities of ASCs which can be the cell depot required in fat graft survival.


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