Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.
10.5045/kjh.2011.46.4.265
- Author:
Hong Bum PARK
1
;
Jeong Hee YANG
;
Kwang Hoe CHUNG
Author Information
1. Department of Applied Bioscience, College of Life Science, CHA University, Sungnam, Korea. hoe@cha.ac.kr
- Publication Type:Original Article
- Keywords:
Platelet rich plasma (PRP);
Wound healing;
Cytokine profile;
Cell proliferation;
Cell migration;
Matrix metalloproteinase
- MeSH:
Blood Platelets;
Cell Movement;
Cell Proliferation;
Chemokines;
Intercellular Signaling Peptides and Proteins;
Matrix Metalloproteinase 1;
Matrix Metalloproteinases;
Platelet-Rich Plasma;
Skin;
Thrombin;
Transcription Factors;
Transducers;
Up-Regulation;
Wound Healing
- From:Korean Journal of Hematology
2011;46(4):265-273
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The underlying rationale of platelet rich plasma (PRP) therapy is that an injection of concentrated PRP at the site of injury may promote tissue repair via cytokine release from platelets. The molecular mechanisms of PRP therapy in the skin wound healing process are not well understood at present, and would benefit from clarification. METHODS: PRP was stimulated with angonists for 5 min, and cytokine profile analysis was performed. To investigate the wound healing activity of PRP, cell proliferation and migration analyses were performed in skin cells. The effects of PRP were analyzed on the expression and activity of matrix metalloproteinase (MMP)-1, -2, -9, and the activation of transcription factors. RESULTS: Thrombin was found to be a strong stimulator of PRP activation to release growth factors and chemokines. PRP induced cell proliferation and migration in HUVECs, HaCaT cells, and HDFs, as well as MMP-1and MMP-9 expression in HaCaT cells, but PRP did not have a significant effect on the expression or activity of MMPs in HDFs. The transcription factors, including signal transducer and activator of transcription-3 (STAT-3) were found to be phosphorylated following PRP treatment in HaCaT cells. CONCLUSION: In this study, we have identified the cytokine profile of activated PRP after agonist stimulation. We have shown that PRP plays an active role in promoting the proliferation and migration of skin cells via the regulation of MMPs, and this may be applicable to the future development of PRP therapeutics to enhance skin wound healing.
