The Effects of Platelet-Rich Plasma on Cell Proliferation and Adipogenic Potential of Adipose-Derived Stem Cells

• Published in: Tissue engineering. Part A Vol. 21; no. 21-22; pp. 2714 - 2722
• Main Authors: Liao, Han Tsung, James, Isaac B., Marra, Kacey G., Rubin, J. Peter
• Format: Journal Article
• Language: English
• Published: United States Mary Ann Liebert, Inc 01.11.2015
• Subjects: Adipocytes - cytology; Adipocytes - physiology; Adipogenesis - physiology; Batch Cell Culture Techniques - methods; Body fat; Cell culture; Cell Differentiation - physiology; Cell growth; Cell Proliferation - physiology; Cells, Cultured; Humans; Original; Original Articles; Plasma; Platelet-Rich Plasma - metabolism; Stem cells; Stem Cells - cytology; Stem Cells - physiology; Tissue engineering
• ISSN: 1937-3341; 1937-335X
• DOI: 10.1089/ten.tea.2015.0159

Background: Platelet-rich plasma (PRP) contains multiple growth factors and has been shown to enhance fat graft survival after lipotransfer. However, the molecular mechanisms mediating this effect remain unknown. Adipose-derived stem cells (ASCs) play an important role in fat graft survival and are a likely target for PRP-mediated effects. This study seeks to investigate the impact of PRP on ASC proliferation and adipogenic differentiation. Methods: Human ASCs were isolated using our laboratory protocol. The experiments were divided into four arms: (1) ASCs cultured in general culture medium alone; (2) ASCs in general culture medium + 5%, 10%, 15%, or 20% PRP; (3) ASCs cultured in adipogenic differentiation medium alone; (4) ASCs cultured in adipogenic medium + 5%, 10%, 15%, or 20% PRP. Cell proliferation was analyzed and comparative m-RNA expression of adipogenic genes was assessed by quantitative PCR. Protein expression was determined by western blot. Results: PRP significantly enhanced proliferation of ASCs, even in the presence of antiproliferative, proadipogenic media. In contrast, PRP inhibited adipogenic differentiation in adipogenic media, evidenced by decreased intracellular lipid accumulation and reduced adipogenic gene expression (PPAR-γ and FABP4). Inhibition appears to occur through downregulation of bone morphogenetic protein receptor IA (BMPRIA) and fibroblast growth factor receptor 1 (FGFR1). Interestingly, PRP elicited these effects across the entire range of doses studied. Conclusions: PRP appears to modulate ASC function primarily by enhancing cell proliferation. The consequences of its impact on adipogenesis are less clear. Enhanced proliferation initially might set the stage for more robust regeneration and adipogenesis at later time points, providing an important target for ongoing research.