Acidic Fibroblast Growth Factor Accelerates Dermal Wound Healing in Diabetic Mice

Mellin, T.N.; Cashen, Doreen E.; Ronan, John; Murphy, Beth S; DiSalvo, Jerry; Thomas, Kenneth A.

doi:10.1111/1523-1747.ep12607026

Cited by 83 publications

(58 citation statements)

References 31 publications

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“…FGFs promote angiogenesis as well as stimulate proliferation of many cell types involved in wound healing, including endothelial cells, fibroblasts, and keratinocytes (4,5). Topical application of FGF1 and FGF2 accelerates wound healing in a number of animal models (29,32). Many of the cell types active in wound healing that are responsive to FGFs are themselves capable of secreting FGFs and other cytokines, raising the possibility of highly complex and regulated interactions between a variety of cell types.…”

mentioning

confidence: 99%

Compensation by Fibroblast Growth Factor 1 (FGF1) Does Not Account for the Mild Phenotypic Defects Observed in FGF2 Null Mice

Miller¹,

Ortega²,

Bashayan

et al. 2000

Molecular and Cellular Biology

286

156

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Fibroblast growth factor 1 (FGF1) and FGF2, the prototypic members of the FGF family of growth factors, have been implicated in a variety of physiological and pathological processes. Unlike most other FGFs, FGF1 and FGF2 are ubiquitously expressed and are not efficiently secreted. Gene knockouts in mice have previously demonstrated a role for FGF2 in brain development, blood pressure regulation, and wound healing. The relatively mild phenotypic defects associated with FGF2 deletion led to the hypothesis that the continued expression of other FGFs partially compensated for the absence of FGF2 in these mice. We now report our generation of mice lacking FGF1 and their use, in combination with our previously described FGF2 null mice, to produce mice lacking both FGF1 and FGF2. FGF1-FGF2 double-knockout mice are viable and fertile and do not display any gross phenotypic defects. In the double-knockout mice we observed defects that were similar in extent to those previously described for the FGF2 null mice. Differences in the organization of neurons of the frontal motor cortex and in the rates of wound healing were observed. We also observed in FGF2 ؊/؊ mice and in FGF1-FGF2 double-knockout mice novel impairments in hematopoiesis that were similar in severity. Essentially no abnormalities were found in mice lacking only FGF1. Our results suggest that the relatively mild defects in FGF2 knockout animals are not a consequence of compensation by FGF1 and suggest highly restricted roles for both factors under normal developmental and physiological conditions. Fibroblast growth factors (FGFs) comprise a widely expressed and multifunctional family of polypeptides. FGFs transduce signals that can regulate cell growth, migration, differentiation, or survival. The biological activity of FGFs is mediated through interactions with transmembrane tyrosine kinase receptors. Four different receptors for FGFs are known, although each is present in multiple isoforms owing to alternative splicing of the mRNA. For the most part, there is no one-to-one correspondence between FGF ligands and receptors. A given FGF may be capable of multiple receptor isoforms; conversely, any receptor variant may bind multiple FGFs (3,8,19).FGF signaling has been implicated in a variety of physiological and pathological processes, ranging from angiogenesis to tumor progression. To date, however, the most clearly demonstrated role of FGF signaling is in development. Studies using knockout mice have demonstrated essential functions for FGF receptor 1 (FGFR1) and FGFR2 in early development (1, 12, 40, 41) and roles for FGFR3 in skeletal morphogenesis (9, 11). Studies of mice lacking individual FGFs reveal a variety of phenotypes which range from early embryonic lethality to very mild defects (14,16,17,22,23,27,30,31,34,42). These findings most likely reflect the redundancy of the FGF family of ligands or their uniqueness of expression in specific tissues.A total of 22 different FGF molecules have been described so far, although four of them (FGF-homologous fa...

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mentioning

confidence: 99%

Compensation by Fibroblast Growth Factor 1 (FGF1) Does Not Account for the Mild Phenotypic Defects Observed in FGF2 Null Mice

Miller¹,

Ortega²,

Bashayan

et al. 2000

Molecular and Cellular Biology

286

156

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“…Morphometry is another method that has been used to study the healing of bone 16 , skin 17 , mesenterium 18 , intestinal anastomosis 19 and abdominal wall 10,20 .…”

Section: Discussionmentioning

confidence: 99%

Comparative study between two techniques of incisional hernia repair with polypropylene mesh in rabbits

et al. 2010

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Purpose:To compare two different incisional hernia repair techniques (repair with a polypropylene mesh reinforcement on the peritonium-aponeurosis versus polypropylene mesh sutured to the borders of the hernial ring as a bridge) in rabbits. Methods: Incisional hernia was experimentally developed through a 4-cm median incision in 60 rabbits. After 30 days, half of the animals were operated for primary wall closure and placement of a polypropylene mesh reinforcement, while the other half had a polypropylene mesh sutured to the borders of the hernial ring as a bridge. Clinical development, scar breaking strength, as well as gross, microscopic and morphometric parameters were evaluated in all animals 30, 60, and 90 days after repair. Results: No significant differences in breaking strength or histological parameters were observed between groups at any time point studied. No statistical difference regarding complications was detected, although denser and firmer adhesions to the abdominal wall were seen after the mesh was placed as a "bridge". Conclusions: No significant differences between the incisional hernia repair techniques assessed were observed regarding breaking strength, and histological and morphometric parameters. The number of complications was similar in both study groups. However, adhesion of abdominal cavity organs to the scar area was much denser after the placement of a mesh to bridge the defect. Key words: Hernia, Ventral. Polypropylenes. Surgical Mesh. Rabbits. RESUMOObjetivo: Comparar duas técnicas de tratamento da hérnia incisional em coelhos utilizando a tela de polipropileno apoiando um reforço peritônio -aponeurótico ou suturada nas bordas do anel herniário 'em ponte". Métodos: Foram operados 60 coelhos para a produção de hérnia incisional, em uma incisão mediana de 4 centímetros. Após 30 dias, metade dos animais foram operados com o fechamento primário da parede, com colocação de uma tela de polipropileno apoiando o reforço e a outra metade dos animais com a colocação da tela suturada nas bordas do anel herniário "em ponte". Os animais foram avaliados com 30 (M1), 60 (M2)e 90 (M3) dias de pós-operatório. Os parâmetros analisados foram a evolução clínica, análise da força de ruptura da cicatriz, estudo macroscópico, análise microscópica e morfométrica. Resultados: Não foram observadas diferenças significantes com relação a força de ruptura e estudos histológicos nos dois grupos e vários momentos estudados. Não houve diferença estatística com relação às complicações, embora os animais que receberam a tela "em ponte" tiveram aderências mais firmes e intensas à parede abdominal. Conclusões: As duas técnicas utilizadas para correção da hérnia incisional em coelhos não mostraram diferenças significantes quanto a força de ruptura, análise histológica e morfométrica. O número de complicações foi semelhante, porém a aderência de órgãos da cavidade abdominal à área de cicatriz foi muito mais intensa no grupo em que a tela foi colocada "em ponte". Descritores: Hérnia Ventral. Polipropilenos.Tel...

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“…47 FGF-1, -2, -7, and -10 have been shown to have both mitogenic and motogenic effects on KCs both in vitro and in vivo. [48][49][50][51][52][53][54][55][56][57] In addition to binding to heparin and heparan sulfate proteoglycans in the ECM, FGFs bind to FGF binding proteins (FGFBP), which release FGFs from the ECM, thereby increasing the pool of free FGFs available for binding to FGFRs. 58 FGF-2 stimulates lamellipodia formation and Rac activation, leading to KC migration, and has a synergistic effect with EGF on inducing KC proliferation.…”

Section: 32mentioning

confidence: 99%

The Roles of Growth Factors in Keratinocyte Migration

Seeger

Paller

2015

Advances in Wound Care

153

126

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Acidic Fibroblast Growth Factor Accelerates Dermal Wound Healing in Diabetic Mice

Cited by 83 publications

References 31 publications

Compensation by Fibroblast Growth Factor 1 (FGF1) Does Not Account for the Mild Phenotypic Defects Observed in FGF2 Null Mice

Compensation by Fibroblast Growth Factor 1 (FGF1) Does Not Account for the Mild Phenotypic Defects Observed in FGF2 Null Mice

Comparative study between two techniques of incisional hernia repair with polypropylene mesh in rabbits

The Roles of Growth Factors in Keratinocyte Migration

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