title: Platelet-rich plasma: growth factors and pro- and anti-inflammatory properties.
abstract: BACKGROUND
  Platelet-rich plasma (PRP) promotes regeneration of bone, presumably through the action of concentrated growth factors. However, it is not clear how PRP affects the inflammatory response. The purpose of this study was to analyze the growth factors in PRP and to study the effects of PRP on monocyte cytokine release and lipoxin A(4) (LXA(4)) generation.
  
  
  METHODS
  PRP was prepared from healthy donors. Platelet-derived growth factor (PDGF)-AB, PDGF-BB, transforming growth factor-beta1, insulin-like growth factor-I, fibroblast growth factor-basic (FGF-b), epidermal growth factor (EGF), vascular endothelial growth factor, interleukin-12 (p40/70), and regulated on activation, normal T-cell expressed and secreted (RANTES) levels were evaluated by enzyme-linked immunosorbent assay and bead-based multiplexing. Peripheral blood monocytes were isolated and cultured with or without PRP. Cytokine, chemokine, and LXA(4) levels as well as monocyte chemotactic migration were analyzed.
  
  
  RESULTS
  Growth factors were increased significantly in PRP compared to whole blood (WB) and platelet-poor plasma. Monocyte chemotactic protein-1 (MCP-1) was suppressed significantly by PRP, whereas RANTES was increased significantly in monocyte cultures. LXA(4) levels were significantly higher in PRP compared to WB. PRP stimulated monocyte chemotaxis in a dose-dependent fashion, whereas RANTES, in part, was responsible for PRP-mediated monocyte migration.
  
  
  CONCLUSIONS
  PRP is a rich source of growth factors and promoted significant changes in monocyte-mediated proinflammatory cytokine/chemokine release. LXA(4) was increased in PRP, suggesting that PRP may suppress cytokine release, limit inflammation, and, thereby, promote tissue regeneration.
authors.affiliation: Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, Boston, MA 02118, USA.
authors.forename: Hesham
authors.initials: H
authors.lastname: El-Sharkawy
authors.forename: Alpdogan
authors.initials: A
authors.lastname: Kantarci
authors.forename: Jennifer
authors.initials: J
authors.lastname: Deady
authors.forename: Hatice
authors.initials: H
authors.lastname: Hasturk
authors.forename: Hongsheng
authors.initials: H
authors.lastname: Liu
authors.forename: Mohammad
authors.initials: M
authors.lastname: Alshahat
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Van Dyke
mesh_terms: D000328:Adult; D018946:Chemokine CCL5 / Q000097:blood; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology*; D044045:Lipoxins / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D010976:Platelet Count; D053657:Platelet-Rich Plasma / Q000737:chemistry* / Q000378:metabolism
chemical_list: D018946:Chemokine CCL5; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D044045:Lipoxins; C040527:lipoxin A4