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Open AccessJournal ArticleDOI

Normal skin and hypertrophic scar fibroblasts differentially regulate collagen and fibronectin expression as well as mitochondrial membrane potential in response to basic fibroblast growth factor.

TLDR
BFGF has differential effects and mechanisms on fibroblasts of the normal skin and hypertrophic scars, indicating that bFGF may play a role in the early phase of skin wound healing and post-burn scar formation.
Abstract
Basic fibroblast growth factor (bFGF) regulates skin wound healing; however, the underlying mechanism remains to be defined. In the present study, we determined the effects of bFGF on the regulation of cell growth as well as collagen and fibronectin expression in fibroblasts from normal human skin and from hypertrophic scars. We then explored the involvement of mitochondria in mediating bFGF-induced effects on the fibroblasts. We isolated and cultivated normal and hypertrophic scar fibroblasts from tissue biopsies of patients who underwent plastic surgery for repairing hypertrophic scars. The fibroblasts were then treated with different concentrations of bFGF (ranging from 0.1 to 1000 ng/mL). The growth of hypertrophic scar fibroblasts became slower with selective inhibition of type I collagen production after exposure to bFGF. However, type III collagen expression was affected in both normal and hypertrophic scar fibroblasts. Moreover, fibronectin expression in the normal fibroblasts was up-regulated after bFGF treatment. bFGF (1000 ng/mL) also induced mitochondrial depolarization in hypertrophic scar fibroblasts (P < 0.01). The cellular ATP level decreased in hypertrophic scar fibroblasts (P < 0.05), while it increased in the normal fibroblasts following treatment with bFGF (P < 0.01). These data suggest that bFGF has differential effects and mechanisms on fibroblasts of the normal skin and hypertrophic scars, indicating that bFGF may play a role in the early phase of skin wound healing and post-burn scar formation.

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Insights into the Pathophysiology of Hypertrophic Scars and Keloids: How Do They Differ?

TL;DR: The clinical presentation of aberrant scars is reviewed and it is illustrated how they can be differentiated and how altered expression levels and the distribution of several factors may contribute to their unique clinical characteristics and presentation.
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Growth factor pathways in hypertrophic scars: Molecular pathogenesis and therapeutic implications.

TL;DR: The therapeutic implications and future challenges of these molecular discoveries are critically discussed in the hope of advancing therapeutic approaches to limit pathological scar formation.
Journal ArticleDOI

Low-molecular-weight fractions of Alcalase hydrolyzed egg ovomucin extract exert anti-inflammatory activity in human dermal fibroblasts through the inhibition of tumor necrosis factor–mediated nuclear factor κB pathway

TL;DR: This study demonstrated that both peptide composition and MW distribution play important roles in anti-inflammatory activity, indicating the responsible role of low-MW bioactive peptides in exerting the beneficial biological function.
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Extracorporeal Shock Wave Therapy Alters the Expression of Fibrosis-Related Molecules in Fibroblast Derived from Human Hypertrophic Scar.

TL;DR: In this article, the authors investigated the mechanism underlying changes in cellular and molecular biology induced by extracorporeal shock wave therapy of fibroblasts derived from scar tissue (HTSFs), and found that suppressed epithelial-mesenchymal transition might be responsible for the anti-scarring effect of ESWT.
Journal ArticleDOI

Chicken collagen hydrolysates differentially mediate anti-inflammatory activity and type I collagen synthesis on human dermal fibroblasts

TL;DR: It is found that the use of two rather than one enzyme for hydrolysis generates a greater abundance of low molecular weight peptides with consequent improvement in bioactive properties.
References
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Journal ArticleDOI

COLLAGENS: Molecular Biology, Diseases, and Potentials for Therapy

TL;DR: The collagen superfamily of proteins now contains at least 19 proteins formally defined as collagens and an additional ten proteins that have collagen-like domains, and a number of experiments suggest it may be possible to inhibit collagen synthesis with oligo-nucleotides or antisense genes.
Journal ArticleDOI

Neuronal defects and delayed wound healing in mice lacking fibroblast growth factor 2.

TL;DR: Results indicate that FGF2, although not essential for embryonic development, plays a specific role in cortical neurogenesis and skin wound healing in mice, which, in spite of the apparent redundancy of FGF signaling, cannot be carried out by other FGF family members.
Journal ArticleDOI

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

TL;DR: It is shown that Col6a1−/− muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum and mitochondria and spontaneous apoptosis, which indicates that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.
Journal Article

Platelet-derived growth factor (BB homodimer), transforming growth factor-beta 1, and basic fibroblast growth factor in dermal wound healing. Neovessel and matrix formation and cessation of repair.

TL;DR: Analysis of the composition, quantity, and rate of extracellular matrix deposition within growth factor-treated lapine ear excisional wounds suggest that specific growth factors may selectively regulate components of the repair response by differing mechanisms, offering the potential for targeted therapeutic intervention.
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