Basic fibroblast growth factor accelerates and improves second‐degree burn wound healing

Akita, Sadanori; Akino, Kozo; Imaizumi, Toshifumi; Hirano, Akiyoshi

doi:10.1111/j.1524-475x.2008.00414.x

Cited by 141 publications

(83 citation statements)

References 29 publications

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“…FGF-2 has also been considered for other therapeutic applications in regenerative medicine. For instance, topical FGF-2 accelerates healing and lessens scarring in patients with second-degree burns (49). FGF-2 has been evaluated for "therapeutic angiogenesis" in patients with refractory angina (50), and shows no nontarget organ effects.…”

Section: Table 1 the Delayed Addition Of Fgf-2 Attenuates Tgf-b-stimmentioning

confidence: 99%

Transforming Growth Factor–β–Induced Differentiation of Airway Smooth Muscle Cells Is Inhibited by Fibroblast Growth Factor–2

Schuliga¹,

Javeed

Harris³

et al. 2013

Am J Respir Cell Mol Biol

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In asthma, basic fibroblast growth factor (FGF-2) plays an important (patho)physiological role. This study examines the effects of FGF-2 on the transforming growth factor-b (TGF-b)-stimulated differentiation of airway smooth muscle (ASM) cells in vitro. The differentiation of human ASM cells after incubation with TGF-b (100 pM) and/ or FGF-2 (300 pM) for 48 hours was assessed by increases in contractile protein expression, actin-cytoskeleton reorganization, enhancements in cell stiffness, and collagen remodeling. FGF-2 inhibited TGF-b-stimulated increases in transgelin (SM22) and calponin gene expression (n ¼ 15, P , 0.01) in an extracellular signal-regulated kinase 1/2 (ERK1/2) signal transduction-dependent manner. The abundance of ordered a-smooth muscle actin (a-SMA) filaments formed in the presence of TGF-b were also reduced by FGF-2, as was the ratio of F-actin to G-actin (n ¼ 8, P , 0.01). Furthermore, FGF-2 attenuated TGF-b-stimulated increases in ASM cell stiffness and the ASM-mediated contraction of lattices, composed of collagen fibrils (n ¼ 5, P , 0.01). However, the TGF-b-stimulated production of IL-6 was not influenced by FGF-2 (n ¼ 4, P . 0.05), suggesting that FGF-2 antagonism is selective for the regulation of ASM cell contractile protein expression, organization, and function. Another mitogen, thrombin (0.3 U ml 21), exerted no effect on TGF-b-regulated contractile protein expression (n ¼ 8, P . 0.05), a-SMA organization, or the ratio of F-actin to G-actin (n ¼ 4, P . 0.05), suggesting that the inhibitory effect of FGF-2 is dissociated from its mitogenic actions. The addition of FGF-2, 24 hours after TGF-b treatment, still reduced contractile protein expression, even when the TGF-b-receptor kinase inhibitor, SB431542 (10 mM), was added 1 hour before FGF-2. We conclude that the ASM cell differentiation promoted by TGF-b is antagonized by FGF-2. A better understanding of the mechanism of action for FGF-2 is necessary to develop a strategy for therapeutic exploitation in the treatment of asthma.Keywords: airway wall remodeling; a-smooth muscle actin; asthma; cytoskeleton; transgelin Airway wall remodeling (AWR) contributes to airway dysfunction in asthma. AWR comprises an array of persistent tissue structural changes that are thought to occur through a process of injury and dysregulated repair, linked to chronic airway inflammation. Features of AWR include the increased deposition of extracellular matrix (ECM), airway smooth muscle (ASM) hyperplasia and hypertrophy, mucous cell metaplasia, and angiogenesis (1). The deposition of collagens I and III in the subepithelial layer and within smooth muscle bundles by airway mesenchyma increases airway wall thickness and reduces airway wall distensibility (2, 3). An effective anti-remodeling treatment is expected to reduce airway reactivity and symptoms in asthma (4, 5).Transforming growth factor-b (TGF-b) is an important mediator of AWR in asthma. TGF-b stimulates ASM cells to differentiate into a more contractile and hypertrophic phenotype (6, 7). TGF-b ...

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Section: Table 1 the Delayed Addition Of Fgf-2 Attenuates Tgf-b-stimmentioning

confidence: 99%

Transforming Growth Factor–β–Induced Differentiation of Airway Smooth Muscle Cells Is Inhibited by Fibroblast Growth Factor–2

Schuliga¹,

Javeed

Harris³

et al. 2013

Am J Respir Cell Mol Biol

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“…118,119 In 1 controlled adult study, topical bFGF resulted in better scar quality and accelerated wound healing. 120 The potential for therapeutic use of bFGF has been studied in the pediatric population. One study showed that children with second-degree burns who received topical bFGF had a significantly enhanced skin/scar color match compared with the placebo group that received only impregnated gauze after 1 year.…”

Section: Basic Fibroblast Growth Factormentioning

confidence: 99%

Scar Management in the Pediatric and Adolescent Populations

Krakowski

Totri

Donelan³

et al. 2016

Pediatrics

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For most children and adolescents who have developed symptomatic scars, cosmetic concerns are only a portion of the motivation that drives them and their caregivers to obtain treatment. In addition to the potential for cosmetic disfigurement, scars may be associated with a number of physical comorbidities including hypertrichosis, dyshidrosis, tenderness/pain, pruritus, dysesthesias, and functional impairments such as contractures, all of which may be compounded by psychosocial factors. Although a plethora of options for treating scars exists, specific management guidelines for the pediatric and adolescent populations do not, and evidence must be extrapolated from adult studies. New modalities such as the scar team approach, autologous fat transfer, and ablative fractional laser resurfacing suggest a promising future for children who suffer symptomatically from their scars. In this state-of-the-art review, we summarize cutting-edge scar treatment strategies as they relate to the pediatric and adolescent populations.

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“…51 Another FGF family cytokine, basic FGF (bFGF) or FGF-2, is primarily found as a potent angiogenic growth factor because of its high capacity for inducing endothelial cell proliferation and migration as well as smooth cell proliferation, 52 and also accelerates second-degree burn wound healing and improves scar quality. 53 In burns, resurfacing with a dermal component is required, and bFGF stimulates wound healing and enhances human skin-derived mesenchymal stem cells under serum-free conditions in a dosedependent manner. 54 In a mini-pig receiving 10-Gy external X-ray radiation to the skin and subcutaneous tissue with a tissue expander underneath the subcutaneous tissue, immediate use of bFGF after radiation successfully protected the tissue from subsequent damage by increasing epithelial proliferation, suppressing the induction of apoptotic cells, and enhancing angiogenic cells.…”

Section: Mitigators Of Radiationmentioning

confidence: 99%