Recombinant human platelet-derived growth factor enhances repair of cutaneous full-thickness excision by increasing the phosphorylation of extracellular signal-regulated kinase in diabetic rat

Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2006 Nov;20(11):1093-8.

Abstract

Objective: To investigate the possible signaling mechanisms by which recombinant human platelet-derived growth factor (rhPDGF) accelerated healing of cutaneous wound in diabetic rats.

Methods: Four full-thickness skin wounds were incised in the back of 26 male Wistar diabetic rats. The wounded rats were divided into 3 groups (7 or 8 rats each group). One group without treatment was used as a control, and the other 2 groups were treated with rhPDGF at a dose of 7.0 microg/cm2 wound or vehicle (DMSO/0.9% NaCl, vol/vol 1:1) from 1 to 14 days. The wound healing was evaluated by the measurements of the wound volume and area. Immunofluorescent and immunohistochemical staining were used to examine the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and the expression of proliferative cell nuclear antigen (PCNA), respectively.

Results: Granulation tissue appeared in the bed of wound after injury. The number of blood capillary buds and fibroblasts was greater in the rhPDGF-treated group than that in the other 2 groups. A lot of inflammatory cells infiltration and collagen deposition were observed in the wound. The wound-volume in the rhPDGF-treated group was smaller than that in control group (P < 0.05). The reepithelialization rate in rhPDGF-treated group was higher than that in the other 2 groups at 7 days after injury (P < 0.05). The expression of PCNA in reparative cells was higher in rhPDGF-treated group than in control group or vehicle-treated group at 3,7 days after injury (P < 0.05). The phosphorylation of ERK1/2 was stronger in rhPDGF-treated group than that in control group or vehicle group at 7 and 14 days after injury (P < 0.05).

Conclusion: These results suggest that rhPDGF accelerates wound healing and improves healing quality by increasing the phosphorylation of ERK1/2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental* / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Male
  • Phosphorylation
  • Platelet-Derived Growth Factor / pharmacology*
  • Rats
  • Rats, Wistar
  • Recombinant Proteins / pharmacology
  • Skin / injuries
  • Wound Healing / drug effects*

Substances

  • Platelet-Derived Growth Factor
  • Recombinant Proteins
  • Extracellular Signal-Regulated MAP Kinases