The effect of growth hormone on fibroblast proliferation and keratinocyte migration

Background: The beneficial effects of growth hormones (GHs) on wound healing have been reported. Although the mechanism of how GH promotes wound healing is unclear, there are reports showing that the principal factor lies in the GH-stimulated production of IGF-1 in topical wounds. In this study, a human primary cell model was devised to examine how the topical application of GHs affects fibroblast proliferation and keratinocyte migration, which play fundamental roles in wound healing. Methods: The fibroblasts were cultured in media with different concentrations of GH. The amount of fibroblast proliferation was assessed using a tetrazolium-based colourimetric assay (MTT assay). The amount of newly formed IGF-1 mRNA was measured by reverse transcription and polymerase chain reaction (RT-PCR). Keratinocyte migration was compared using a migration assay. Results: Fibroblast proliferation was significantly higher in the experimental group than in the control group (the absorbance of 2.5 IU L(-1) GH applied group: 0.3954 +/- 0.056, control group: 0.2943 +/- 0.0554, P < 0.05), and the promotion of IGF-1 formation by fibroblasts was observed. There was more keratinocyte migration in the experimental group than in the control group (the remaining gap in the 2.5 IU L(-1) GH applied group after keratinocyte migration: 46.57 +/- 2.22% of the primary gap, control group: 75.14 +/- 3.44%, P < 0.05). Conclusion: GH enhances the local formation of IGF-1, which activates fibroblast proliferation and keratinocyte migration. These results highlight the potential of the topical application of GHs in the treatment of wounds. (C) 2009 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.LI JX, 2006, ZHONGHUA SHAO SHANG, V22, P33Jeschke MG, 2005, WOUND REPAIR REGEN, V13, P269Li W, 2004, J INVEST DERMATOL, V123, P622, DOI 10.1111/j.0022-202X.2004.23416.xThorey IS, 2004, J BIOL CHEM, V279, P26674, DOI 10.1074/jbc.M311467200Dunaiski V, 2002, GROWTH HORM IGF RES, V12, P381, DOI 10.1016/S1096-6374(02)00080-1Losada F, 2002, WORLD J SURG, V26, P2Singer AJ, 1999, NEW ENGL J MED, V341, P738Guicheux J, 1998, BONE, V22, P25PIERRE EJ, 1997, J BURN CARE REHABIL, V18, P287ROBERTSON JG, 1997, WOUND REPAIR REGEN, V5, P168JORGENSEN PH, 1996, WOUND REPAIR REGEN, V4, P40STEENFOS HH, 1994, SCAND J PLAST RECONS, V28, P95RASMUSSEN LH, 1994, WOUND REPAIR REGEN, V2, P31PELL JM, 1992, ENDOCRINOLOGY, V130, P1942STEENFOS HH, 1992, J ENDOCRINOL, V132, P293MERCHAV S, 1988, BRIT J HAEMATOL, V70, P267GREEN H, 1985, DIFFERENTIATION, V29, P195SCOTT CD, 1985, ENDOCRINOLOGY, V116, P1094KURTZ A, 1985, J CLIN INVEST, V76, P1643MOSMANN T, 1983, J IMMUNOL METHODS, V65, P55BOYCE ST, 1983, J INVEST DERMATOL S, V81, P33DIEGELMANN RF, 1979, J CELL PHYSIOL, V98, P341