UVA irradiation following treatment with topical 8-methoxypsoralen improves bleomycin-induced scleroderma in a mouse model, by reducing the collagen content and collagen gene expression levels in the skin

Hayashi, Shujiro; Ikeda, Masashi; Kitamura, Yohei; Hamasaki, Yoichiro; Hatamochi, Atsushi

doi:10.1016/j.jdermsci.2012.02.013

Cited by 11 publications

(9 citation statements)

References 12 publications

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“…They also showed that collagenase mRNA expression and activity in the fibroblast conditioned medium is significantly reduced in HSC fibroblasts compared to the normal ones [4]. Recent studies [5], [6], [7] demonstrate that localized application of agents that are targeted to suppress matrix accumulation provide an approach to specifically reduce scarring.…”

Section: Introductionmentioning

confidence: 99%

Anti-Scarring Properties of Different Tryptophan Derivatives

et al. 2014

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Hypertrophic scars are associated with prolonged extracellular matrix (ECM) production, aberrant ECM degradation and high tissue cellularity. Routinely used antifibrotic strategies aim to reduce ECM deposition and enhance matrix remodeling. Our previous study investigating the antifibrotic effects of indoleamine2, 3 dioxygenase (IDO) led to the identification of kynurenine (Kyn) as an antiscarring agent. A topical antifibrogenic therapy using Kyn is very attractive; however, it is well established that Kyn passes the blood brain barrier (BBB) which causes complications including excitatory neuronal death. Here we investigated the antiscarring properties of kynurenic acid (KynA), a downstream end product of Kyn that is unlikely to pass the BBB, as an effective and safe replacement for Kyn. Our results indicated that while not having any adverse effect on dermal cell viability, KynA significantly increases the expression of matrix metalloproteinases (MMP1 and MMP3) and suppresses the production of type-I collagen and fibronectin by fibroblasts. Topical application of cream containing KynA in fibrotic rabbit ear significantly decreased scar elevation index (1.13±0.13 vs. 1.61±0.12) and tissue cellularity (221.38±21.7 vs. 314.56±8.66 cells/hpf) in KynA treated wounds compared to controls. KynA treated wounds exhibited lower levels of collagen deposition which is accompanied with a significant decrease in type-I collagen and fibronectin expression, as well as an increase in MMP1 expression compared to untreated wounds or wounds treated with cream only. The results of this study provided evidence for the first time that KynA is promising candidate antifibrogenic agent to improve healing outcome in patients at risk of hypertrophic scarring.

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Section: Introductionmentioning

confidence: 99%

Anti-Scarring Properties of Different Tryptophan Derivatives

et al. 2014

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“…High tissue cellularity and excessive ECM accumulation are among the main characteristics of these pathological conditions . Local application of therapeutic modalities that suppress the ECM accumulation either by the reduction of ECM deposition or by the stimulation of ECM degradation showed promising results in the treatment of fibrotic diseases …”

Section: Introductionmentioning

confidence: 99%

Development of a nanofibrous wound dressing with an antifibrogenic properties in vitro and in vivo model

Poormasjedi‐Meibod

Pakyari

Jackson

et al. 2016

J Biomedical Materials Res

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Dermal fibrosis, characterized by excessive extracellular matrix (ECM), is a pathological condition with limited effective therapeutic modalities. Lack of an antiscarring dressing further impedes the preventive measures for this condition. Here, we develop a new antiscarring dressing and investigate its potential as a slow-releasing vehicle for kynurenic acid (KynA), an antifibrotic agent. KynA was incorporated into polymethyl methacrylate (PMMA) nanofibers, containing increasing concentration of polyethylene glycol (PEG). Fibre morphology, water absorption capacity, surface hydrophilicity, in vitro drug release profile, and in vivo antifibrotic effects were investigated. Increasing concentrations of PEG (1-20%) significantly increased surface hydrophilicity, water absorption capacity, and drug release. Based on the obtained release profiles, PMMA + 10% PEG was the preferred formulation for sustained KynA release up to 120 hours. In vitro studies confirmed the preservation of KynA antifibrotic properties during electrospinning, indicated by fibroblasts proliferation suppression and ECM expression modulation. In vivo application of KynA-incorporated films significantly inhibited collagen (23.89 ± 4.79 vs. 6.99 ± 0.41, collagen-I/β-actin mRNA expression, control vs. treated) and fibronectin expression (7.18 ± 1.09 vs. 2.31 ± 0.05, fibronectin/β-actin mRNA expression, control vs. treated) and enhanced the production of an ECM-degrading enzyme (2.03 ± 0.88 vs. 11.88 ± 1.16 MMP-1/β-actin mRNA expression, control vs. treated). The fabricated KynA-incorporated films can be exploited as antifibrotic wound dressings. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 2334-2344, 2016.

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“…In mice models, UVA1 radiation reduces fibroblast proliferation in a dose-dependent fashion [10, 11]. Additionally, UVA1 radiation administered three times a week showed decreased hydroxyproline and collagen levels in a dose-dependent fashion [11].…”

Section: Mechanism Behind Phototherapeutic Modalities Used In Sclerodmentioning

confidence: 99%

“…On the other hand, in patients with morphea treated with PUVA, there was a fall in serum VCAM molecules and an increase in TNF-α in most patients [30]. In a bleomycin-induced scleroderma rat model, PUVA treatment reduced dermal thickness and hydroxyproline content and downregulated expression of type I and III collagen genes [10]. In one patient with SSc, treatment with oral PUVA therapy three times a week for 4 weeks resulted in loosening of collagen, reduction in edema, and decreased CD34 + cells [31].…”

Section: Mechanism Behind Phototherapeutic Modalities Used In Sclerodmentioning

confidence: 99%

Phototherapy in Scleroderma

Hassani

Feldman

2016

Dermatol Ther (Heidelb)

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Systemic and localized scleroderma are difficult to manage diseases with no accepted gold standard of therapy to date. Phototherapeutic modalities for scleroderma show promise. A PubMed search of information on phototherapy for scleroderma was conducted. The information was classified into effects on pathogenesis and clinical outcomes. Studies on photopheresis were excluded. There were no randomized, double-blind, placebo-controlled studies, and only three controlled studies. The vast majority of identified studies evaluated ultraviolet A1 (UVA1) phototherapy. More rigorous studies are needed to evaluate phototherapy in the treatment of scleroderma. Based on the limited studies available, 20–50 J/cm2 of UVA1 therapy 3–4 times a week for 30 treatments is recommended.

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UVA irradiation following treatment with topical 8-methoxypsoralen improves bleomycin-induced scleroderma in a mouse model, by reducing the collagen content and collagen gene expression levels in the skin

Cited by 11 publications

References 12 publications

Anti-Scarring Properties of Different Tryptophan Derivatives

Anti-Scarring Properties of Different Tryptophan Derivatives

Development of a nanofibrous wound dressing with an antifibrogenic properties in vitro and in vivo model

Phototherapy in Scleroderma

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