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. 2009 Sep;15(3):431-5.
doi: 10.1089/ten.tec.2008.0534.

Buffered platelet-rich plasma enhances mesenchymal stem cell proliferation and chondrogenic differentiation

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Buffered platelet-rich plasma enhances mesenchymal stem cell proliferation and chondrogenic differentiation

Allan Mishra et al. Tissue Eng Part C Methods. 2009 Sep.

Abstract

The success of tissue engineering applications can potentially be dramatically improved with the addition of adjuncts that increase the proliferation and differentiation of progenitor or stem cells. Platelet-rich plasma (PRP) has recently emerged as a potential biologic tool to treat acute and chronic tendon disorders. The regenerative potential of PRP is based on the release of growth factors that occurs with platelet rupture. Its autologous nature gives it a significant advantage in tissue engineering applications. To test whether PRP may be useful specifically for cartilage regeneration, a cell culture experiment was devised in which mesenchymal stem cells (MSCs) were grown in control media or media enhanced with inactivated, buffered PRP. Proliferation 7 days after PRP treatment was increased: 1.041 versus 0.199 for the control media cells ( p<0.001). The messenger RNA (mRNA) level of the osteogenic marker RUNX2 was 52.84 versus 26.88 for the control group ( p<0.005). Likewise the mRNA level of the chondrogenic markers Sox-9 and aggrecan was 29.74 versus 2.29 for the control group ( p<0.001) and 21.04 versus 1.93 ( p<0.001), respectively. These results confirm that PRP enhances MSC proliferation and suggest that PRP causes chondrogenic differentiation of MSC in vitro.

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Figures

FIG. 1.
FIG. 1.
Daily cell numbers over 7 days as a function of PRP concentration in human fibroblasts.
FIG. 2.
FIG. 2.
The 7-day time-point was repeated six times with 10% PRP and compared to control. A 3.3-fold increase in cell number was observed.
FIG. 3.
FIG. 3.
Treatment with 10% inactivated PRP results in a fivefold increase in proliferation after 7 days (p < 0.001).
FIG. 4.
FIG. 4.
PRP treatment causes an increase in expression of markers of both chondrogenic and osteogenic differentiation by human MSCs.

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