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Exp Cell Res. 2017 Mar 1;352(1):146-156. doi: 10.1016/j.yexcr.2017.02.012. Epub 2017 Feb 13.

Platelet rich plasma (PRP) induces chondroprotection via increasing autophagy, anti-inflammatory markers, and decreasing apoptosis in human osteoarthritic cartilage.

Author information

1
Regenerative medicine and inflammation Laboratory, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: Moussa-mayssam@hotmail.com.
2
Research Centre in Osteoarthritis, Research Centre in Monteral University, Canada. Electronic address: daniel.lajeunesse@umontreal.ca.
3
Cancer and metabolism Laboratory, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: George2266@gmail.com.
4
Regenerative medicine and inflammation Laboratory, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: oulaatat@hotmail.com.
5
Hotel Dieu de France, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: Gaby.haykal@hdf.usj.edu.lb.
6
Regenerative medicine and inflammation Laboratory, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: rim.basbous@gmail.com.
7
Carantina Hospital, Beirut, Lebanon. Electronic address: Mava.o@hotmail.com.
8
Regenerative medicine and inflammation Laboratory, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: charbelk3@hotmail.com.
9
Regenerative medicine and inflammation Laboratory, Faculty of Medicine, Saint-Joseph University, Beirut, Lebanon. Electronic address: Nada.aladdin@gmail.com.

Abstract

OBJECTIVES:

Autophagy constitutes a defense mechanism to overcome aging and apoptosis in osteoarthritic cartilage. Several cytokines and transcription factors are linked to autophagy and play an important role in the degradative cascade in osteoarthritis (OA). Cell therapy such as platelet rich plasma (PRP) has recently emerged as a promising therapeutic tool for many diseases including OA. However, its mechanism of action on improving cartilage repair remains to be determined. The purpose of this study is to investigate the effect of PRP on osteoarthritic chondrocytes and to elucidate the mechanism by which PRP contributes to cartilage regeneration.

METHODS:

Osteoarthritic chondrocytes were co-cultured with an increasing concentration of PRP obtained from healthy donors. The effect of PRP on the proliferation of chondrocytes was performed using cell counting and WST8 proliferation assays. Autophagy, apoptosis and intracellular level of IL-4, IL-10, and IL-13 were determined using flow cytometry analyses. Autophagy markers BECLIN and LC3II were also determined using quantitative polymerase chain reaction (qPCR). qPCR and ELISA were used to measure the expression of ADAMDTS-5, MMP3, MMP13, TIMP-1-2-3, aggregan, Collagen type 2, TGF-β, Cox-2, Il-6, FOXO1, FOXO3, and HIF-1 in tissues and co-cultured media.

RESULTS:

PRP increased significantly the proliferation of chondrocytes, decreased apoptosis and increased autophagy and its markers along with its regulators FOXO1, FOXO3 and HIF-1 in osteoarthritic chondrocytes. Furthermore, PRP caused a dose-dependent significant decrease in MMP3, MMP13, and ADAMTS-5, IL-6 and COX-2 while increasing TGF-β, aggregan, and collagen type 2, TIMPs and intracellular IL-4, IL-10, IL-13.

CONCLUSION:

These results suggest that PRP could be a potential therapeutic tool for the treatment of OA.

KEYWORDS:

Anti-inflammatory cytokines; Apoptosis; Autophagy; Osteoarthritis; Platelet rich plasma

PMID:
28202394
DOI:
10.1016/j.yexcr.2017.02.012
[Indexed for MEDLINE]
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