Platelet-derived growth factor levels in wounds of diabetic rats

Doxey, Deborah L.; Ng, May C.; Dill, Russell E.; Iacopino, Anthony M.

doi:10.1016/0024-3205(95)02056-o

Cited by 101 publications

(68 citation statements)

References 26 publications

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“…PDGF functions in a macrophage autocrine feedback loop to stimulate the synthesis and release of growth factors and cytokines. 15 PDGF also stimulates a variety of mesenchymal-derived cell types to enhance DNA synthesis, increase collagen deposition, and stimulate synthesis of extracellular matrix. 16 In synergy with stromal-derived factor-1 (SDF-1), PDGF-BB promotes bone marrow cell growth and resistance to a-interferon-2a-induced apoptosis, 17 suggesting that PDGF and SDF-1 may act in synergy in promoting the self-renewal and survival capacity of bone marrow stromal stem cells.…”

mentioning

confidence: 99%

Recombinant human platelet‐derived growth factor BB (rhPDGF‐BB) and beta‐tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model

Al-Zube

Breitbart

O’Connor

et al. 2009

Journal Orthopaedic Research

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Diabetes mellitus is a common systemic disease that has been associated with poor fracture healing outcomes. The mechanism through which diabetes impairs bone regeneration is unknown. One possible mechanism may be related to either decreased or uncoordinated release of local growth factors at the fracture site. Indeed, previous studies have found reduced platelet-derived growth factor (PDGF) levels in the fracture callus of diabetic rats, suggesting that local application of PDGF may overcome the negative effects of diabetes and promote fracture healing. To test this hypothesis, low (22 mg) and high (75 ug) doses of recombinant human PDGF-BB (rhPDGF-BB) were applied directly to femur fracture sites in BB Wistar diabetic rats that were then compared to untreated or vehicle-treated animals. rhPDGF-BB treatment significantly increased early callus cell proliferation compared to that in control specimens. Low dose rhPDGF-BB treatment significantly increased callus peak torque values (p < 0.05) at 8 weeks after fracture as compared to controls. High dose rhPDGF-BB treatment increased callus bone area at 12 weeks postfracture. These data indicate that rhPDGF-BB treatment ameliorates the effects of diabetes on fracture healing by promoting early cellular proliferation that ultimately leads to more bone formation. Local application of rhPDGF-BB may be a new therapeutic approach to treat diabetes-impaired fracture healing. ß

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mentioning

confidence: 99%

Recombinant human platelet‐derived growth factor BB (rhPDGF‐BB) and beta‐tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model

Al-Zube

Breitbart

O’Connor

et al. 2009

Journal Orthopaedic Research

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“…Vascular endothelial growth factor (VEGF) is a multifunctional growth factor produced by endothelial cells, fibroblasts, smooth muscle cells, trombocytes, neutrophils and macrophages.Its function is to elicit proliferation, migration and differentiation of the said cells (24)(25)(26).Studies on wound healing process in experimentally diabetic animals have shown that several growth factors, including VEGF, are dramatically decreased (27)(28)(29).It has been suggested that administration of VEGF-A via protein or gene transfer methods increases granulation tissue formation, angiogenesis and matrix deposition in experimentally diabetic mice (27).…”

Section: Introductionmentioning

confidence: 99%

“…Fibroblast growth factor (FGF) demonstrates strong mitogenic properties in fibroblasts, osteoblasts, smooth muscle cells, endothelial cells, chondrocytes and melanocytes (27)(28)(29)(30).It is one of the most important growth factors playing crucial roles in embryonic development, angiogenesis and wound healing.Biologically, it acts via binding to the cellular surface receptors belonging to the tyrosine kinase receptor family. Four of such surface receptors (FGFR 1-4) have been identified up until now (31)(32)(33).It has been clearly demonstrated in previous studies that FGFR3 is localized in the suprabasal region of epidermis, in the inner epidermal root sheat of hair follicles, in the smooth musle cells of blood vessels of the normal skin tissue whereas FGFR3 is immunolocalized in the suprabasal and basal layers of epidermis, around the blood vessels of the granulation tissue, in fibroblasts and inflammatory cells of the skin during wound healing process (33).However, the number of histopathological studies on VEGF immunolocalization is still limited while there exist no studies on FGFR-3 in wound healing process in diabetic subjects.…”

Section: Introductionmentioning

confidence: 99%

Investigation of The Wound Healing Effects of Chitosan on FGFR3 and VEGF Immunlocalization in Experimentally Diabetic Rats

İnan¹

2013

IJBMR

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Abstract:Chitosan is a naturally occurring substance that stimulates correct deposition, assembly and orientation of collagen fibres in extracellular matrix components in wounds and promotes migration of inflammatory cells. Fibroblast growth factor (FGF) is one of the most important growth factors playing crucial roles in angiogenesis and wound healing. Biologically, it acts via binding to the cellular surface receptors. FGFR3 is one of the most important receptors. Therefore the aim of the present study was to investigate, histologically and histochemically, the effect of chitosan on wound healing in experimentally diabetic rats divided into four groups. When compared to the diabetic and the control groups, chitosan group had more inflammatory cells, endothelial cells, newly formed blood vessels and reticular -collagen fibres in the wound healing area from the third day of operation.Moreover, in Chitosan Group, stronger VEGF and FGFR3 immunolocalizations were evident and all steps of wound healing process were more regular. FGFR3 antibody used in this study had been tested only on diabetic wound healing. In conclusion, we have concluded that application of chitosan was essential to accelarate wound healing process in diabetic patients.

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“…No DM o processo de cicatrização encontra-se alterado por diversos fatores com supressão de reações inflamatórias, diminuição da angiogênese, alteração na proliferação de queratinócitos, fibroblastos e células endoteliais, aumento na apoptose de queratinócitos e células endoteliais, diminuição na migração de fibroblastos, defeitos na deposição de colágeno e diminuição na produção de fatores de crescimento (Goodson e Hunt, 1977;Werner et al, 1994;BaumgartenerParzer et al, 1995;Doxey et al, 1995;Mehlen et al, 1996;Tanaka et al, 1996;Shaw et al, 1997;Hehenberger et al, 1998;Spravchicov et a., 2001;Loots 2002;Lerman et al, 2003;Deveci et al, 2005). Além disso, a doença vascular periférica e neuropatia também influenciam negativamente a reparação tecidual (Lerman et al, 2003).…”

Section: A Cicatrização No Diabetes Mellitusunclassified

Terapia com laser em baixa intensidade na prevenção dos efeitos causados pela elevada concentração de glicose na proliferação e migração de fibroblastos

Ramalho¹

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Diabetic complications, including wound healing deficiency, are usually associated to chronic hyperglycemia, which leads to oxidative stress and aleatory protein glycation. The aim of this study was to evaluate the effects of high glucose concentrations (HGC) on proliferation, migration and death of cultured fibroblasts, as well as the potential effect of low intensity laser therapy (LILT) (660 and 780 nm; 40mW; 2, 5, 10 and 30J/cm 2 ) preventing these effects. HGC reduced cell proliferation in about 40%, cell migration in about 50% and increased cell death in 30%. Daily irradiation at 660nm and 10J/cm 2 was efficient preventing the effects on cell proliferation and migration. HGC also increased the production of reactive oxygen species, an effect totally prevented by LILT. The results suggest that LILT favors cell proliferation and migration, processes very important for healing, possibly through an anti-oxidant effect.KEY WORDS: Diabetes Mellitus, wound healing, LILT. Organization). Está associado a uma insuficiência da insulina, que pode ser causada tanto pela baixa produção de insulina pelo pâncreas, como pela falta de resposta dos tecidos periféricos a este hormônio, resultando num aumento no nível sanguíneo de glicose (hiperglicemia) (Neville et al., 1995;Robbins et al., 1989). Os níveis sanguíneos normais de glicose situam-se entre 70 e 120mg/dl; em indivíduos diabéticos, estes níveis encontram-se frequentemente entre 200 e 400 mg/dl. O DM é geralmente dividido em dois grupos: insulina-dependente (DMID) outipo I e não insulina-dependente (DMNID), ou tipo II. O DMID é caracterizado por uma deficiência acentuada na produção de insulina, geralmente desde a infância (Neville et al., 1995;Robbins et al., 1989). Os indivíduos geralmente apresentam hiperglicemia intensa e cetoacidose, necessitando de injeções de insulina exógena para sobreviver. O DMNID é mais freqüente em adultos e pessoas obesas e está associado a uma baixa responsividade à insulina. Embora a hiperglicemia esteja presente, a cetoacidose raramente se desenvolve (Neville et al., 1995;Robbins et al., 1989).O DM é uma doença importante quando se consideram as inúmeras complicações dele decorrentes e o seu impacto econômico na sociedade. A causa mais comum de hospitalização de indivíduos diabéticos provém de feridas crônicas, de difícil cicatrização e com recorrência de infecções (Frykberg, 1999).Uma das principais complicações é a doença vascular periférica, devido à microangiopatia, que pode resultar num acometimento isquêmico dos membros. A isquemia predispõe o indivíduo a infecções graves, como por exemplo, a gangrena, que pode gerar uma necessidade de amputação do membro. A cada ano, 20.000 amputações de membros inferiores são realizadas nos EUA devido a complicações gangrenosas do DM (Neville et al., 1995). Os mecanismos envolvidos nesta 12 complicação, no entanto, não estão completamente elucidados (Greenhalgh, 2003). Além da microangiopatia, outras complicações como neuropatia, retinopatia e falência de órgãos, como por exemplo, os ...

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Platelet-derived growth factor levels in wounds of diabetic rats

Cited by 101 publications

References 26 publications

Recombinant human platelet‐derived growth factor BB (rhPDGF‐BB) and beta‐tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model

Recombinant human platelet‐derived growth factor BB (rhPDGF‐BB) and beta‐tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model

Investigation of The Wound Healing Effects of Chitosan on FGFR3 and VEGF Immunlocalization in Experimentally Diabetic Rats

Terapia com laser em baixa intensidade na prevenção dos efeitos causados pela elevada concentração de glicose na proliferação e migração de fibroblastos

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