BACKGROUND: Growth factors have been shown to improve healing in impaired models but not after malnutrition. The effects of growth factors on altered tissue repair caused by malnutrition were examined. METHODS: Nondiabetic and diabetic mice fed a 1% protein diet received full-thickness skin wounds. Wounds were treated topically with vehicle, platelet-derived growth factor (PDGF, 10 micrograms) or basic fibroblast growth factor (bFGF, 1 microgram), for 5 days. RESULTS: Malnourished animals developed significantly impaired wound closure. PDGF or bFGF did not enhance closure in nondiabetic C57BL/KsJ-db/m mice, whether fed normal or restricted diets. The same treatment regimen was effective in reversing the delayed wound closure in their genetically diabetic C57BL/KsJ-db/db littermates. The growth factors significantly enhanced tissue repair in diabetic mice fed a 1% protein diet starting as early as day 15 and continuing until day 21. Protein-depleted diabetic wounds had significantly decreased cellularity and granulation tissue formation. These deficiencies were reversed with growth factor treatment. CONCLUSIONS: Despite the lack of effects in nondiabetic animals, growth factors improve healing in diabetic mice with restricted protein intake. The differential effects may result from different healing mechanisms: nondiabetic animals heal mainly by contraction; diabetic animals require granulation tissue formation and reepithelialization.
BACKGROUND: Growth factors have been shown to improve healing in impaired models but not after malnutrition. The effects of growth factors on altered tissue repair caused by malnutrition were examined. METHODS:Nondiabetic and diabeticmice fed a 1% protein diet received full-thickness skin wounds. Wounds were treated topically with vehicle, platelet-derived growth factor (PDGF, 10 micrograms) or basic fibroblast growth factor (bFGF, 1 microgram), for 5 days. RESULTS: Malnourished animals developed significantly impaired wound closure. PDGF or bFGF did not enhance closure in nondiabetic C57BL/KsJ-db/m mice, whether fed normal or restricted diets. The same treatment regimen was effective in reversing the delayed wound closure in their genetically diabetic C57BL/KsJ-db/db littermates. The growth factors significantly enhanced tissue repair in diabeticmice fed a 1% protein diet starting as early as day 15 and continuing until day 21. Protein-depleted diabetic wounds had significantly decreased cellularity and granulation tissue formation. These deficiencies were reversed with growth factor treatment. CONCLUSIONS: Despite the lack of effects in nondiabetic animals, growth factors improve healing in diabeticmice with restricted protein intake. The differential effects may result from different healing mechanisms: nondiabetic animals heal mainly by contraction; diabetic animals require granulation tissue formation and reepithelialization.
Authors: T Kälicke; O Sprutacz; U Schlegel; F Kutscha-Lissberg; M Köller; G Printzen; G Muhr; S Arens Journal: Unfallchirurg Date: 2004-03 Impact factor: 1.000
Authors: Philip Bao; Arber Kodra; Marjana Tomic-Canic; Michael S Golinko; H Paul Ehrlich; Harold Brem Journal: J Surg Res Date: 2008-05-12 Impact factor: 2.192
Authors: Shin Ae Park; Vijay Krishna Raghunathan; Nihar M Shah; Leandro Teixeira; Monica J Motta; Jill Covert; Richard Dubielzig; Michael Schurr; Roslyn Rivkah Isseroff; Nicholas L Abbott; Jonathan McAnulty; Christopher J Murphy Journal: PLoS One Date: 2014-08-14 Impact factor: 3.240