title: Effects of platelet-rich and -poor plasma on the reparative response of gingival fibroblasts.
abstract: OBJECTIVE
  Although platelet-rich plasma (PRP) has been proposed as a therapeutic tool to enhance wound repair, the cellular and molecular mechanisms stimulated by this agent are still not completely understood. The present study was designed to characterize the effects of PRP and platelet-poor plasma (PPP) supernatants on cell responses involved in gingival tissue repair.
  
  
  METHODS
  We studied the response of human gingival fibroblasts (HGF) to PRP and PPP fractions on: matrix contraction, cell migration, myofibroblastic differentiation, production of matrix components and proteolytic enzymes. PRP and PPP were obtained from donors using a commercial kit. Matrix contraction was evaluated by means of collagen lattices in the presence of matrix metalloproteinase (MMP) and actin polymerization inhibitors. The production of matrix molecules and proteinases was assessed through Western-blot. RhoA activity was evaluated through a pull-down assay. Actin distribution and focal adhesions were assessed through immunofluorescence. Transforming growth factor-beta (TGF-β) was quantified through ELISA.
  
  
  RESULTS
  Both PRP and PPP stimulated human gingival fibroblasts-populated collagen gel contraction and Ilomastat and cytochalasin D inhibited this response. PRP and PPP also stimulated MT1-MMP and TIMP-2 production, RhoA activation and actin cytoskeleton remodeling, cell migration/invasion and myofibroblastic differentiation. TGF-β1 was found at significantly higher concentrations in PRP than in PPP.
  
  
  CONCLUSIONS
  Both PRP and PPP promote wound tissue remodeling and contraction through the stimulation of actin remodeling, the activity of MMPs, promotion of cell migration, and myofibroblastic differentiation. The similar biological responses induced by PRP and PPP suggest that both platelet-derived fractions may exert a positive effect on gingival repair.
authors.affiliation: Laboratory of Periodontal Physiology, Dentistry Academic Unit, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
authors.forename: Mónica
authors.initials: M
authors.lastname: Cáceres
authors.forename: Constanza
authors.initials: C
authors.lastname: Martínez
authors.forename: Jorge
authors.initials: J
authors.lastname: Martínez
authors.forename: Patricio C
authors.initials: PC
authors.lastname: Smith
mesh_terms: D000199:Actins / Q000032:analysis; D000328:Adult; D015153:Blotting, Western; D002454:Cell Differentiation / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D015638:Cytochalasin D / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D005347:Fibroblasts / Q000187:drug effects*; D005881:Gingiva / Q000166:cytology* / Q000187:drug effects*; D006801:Humans; D006877:Hydroxamic Acids; D007211:Indoles / Q000494:pharmacology; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis; D008297:Male; D020782:Matrix Metalloproteinases / Q000494:pharmacology; D053657:Platelet-Rich Plasma / Q000502:physiology*; D018709:Statistics, Nonparametric; D016212:Transforming Growth Factor beta / Q000032:analysis; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D000199:Actins; D006877:Hydroxamic Acids; D007211:Indoles; D036341:Intercellular Signaling Peptides and Proteins; D016212:Transforming Growth Factor beta; D015638:Cytochalasin D; D020782:Matrix Metalloproteinases; C119203:ilomastat