The Most Current Algorithms for the Treatment and Prevention of Hypertrophic Scars and Keloids

Ogawa, Rei

doi:10.1097/prs.0b013e3181c82dd5

Cited by 287 publications

(221 citation statements)

References 55 publications

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“…11 One of the most common treatments is intralesional injection of triamcinolone, which was shown to increase the production of fibroblast growth factor-2 (FGF-2; basic fibroblast growth factor) and decrease the production of transforming growth factor-b (TGF-b) by human dermal fibroblasts. 12 We previously demonstrated that FGF-2 released at the time of adipose injury promotes hepatocyte growth factor (HGF) secretion from adipose-derived stromal cells and/or fibroblasts and inhibits post-injury fibrogenesis.…”

mentioning

confidence: 99%

Therapeutic potential of fibroblast growth factor-2 for hypertrophic scars: upregulation of MMP-1 and HGF expression

Eto

Suga

Aoi

et al. 2012

Laboratory Investigation

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Although hypertrophic scars (HTSs) and keloids are challenging problems, their pathogenesis is not well understood, making therapy difficult. We showed that matrix metalloproteinase (MMP)-1 expression was downregulated in HTS compared with normal skin from the same patients, whereas type 1 and 3 collagen and transforming growth factor-b (TGF-b) were upregulated. These differences, however, were not seen in cultured fibroblasts, suggesting the involvement of microenvironmental factors in the pathogenesis of HTS. Fibroblast growth factor-2 (FGF-2) highly upregulated the expression of MMP-1 and hepatocyte growth factor (HGF) in both HTS-derived and control fibroblasts; the upregulation was reversed by extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) inhibitors. An animal study using human HTS tissue implanted into nude mice indicated that controlled-release FGF-2 resulted in significantly less weight and decreased hydroxyproline content in HTS. Degradation of collagen fibers in FGF-2-treated HTS was also confirmed histologically. Western blotting showed that FGF-2-treated HTS expressed significantly higher MMP-1 protein than control. Decreased MMP-1 expression may be an important transcriptional change in HTS, and its reversal as well as upregulation of HGF by FGF-2 could be a new therapeutic approach for HTS.

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mentioning

confidence: 99%

Therapeutic potential of fibroblast growth factor-2 for hypertrophic scars: upregulation of MMP-1 and HGF expression

Eto

Suga

Aoi

et al. 2012

Laboratory Investigation

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“…10 These basic findings recapitulate well clinical resistance of keloids to various treatments. 11,12 Therefore, we consider that research using KDFs and NDFs is a powerful strategy to characterize the pathological mechanism of keloids as a clue to provide new targets for treatment.…”

mentioning

confidence: 99%

Identification and Characterization of Cartilage Oligomeric Matrix Protein as a Novel Pathogenic Factor in Keloids

Inui

Shono

Nakajima

et al. 2011

The American Journal of Pathology

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To elucidate pathogenic molecules in keloids, microarray analysis was performed using RNAs extracted from keloid-derived fibroblasts and normal skin-derived fibroblasts from the same patient with a typical keloid. Among 11 up-regulated extracellular matrix genes, cartilage oligomeric matrix protein (COMP) was most prominently increased. Up-regulation of COMP mRNA and protein was confirmed in the keloid tissue by quantitative RT-PCR and Western blot. Using immunohistochemistry, we compared 15 keloids and 6 control normal tissues using a COMPspecific antibody and found that COMP stained positively in 10 keloids (66.7%), whereas no staining was observed in normal tissues, demonstrating the ectopic expression of COMP in keloids. Comparing keloids smaller or larger than 10 cm 2 , the larger keloids were significantly more intensely stained with the COMP-specific antibody. Because COMP reportedly accelerates collagen type I fibril assembly, we examined whether extracellular type I collagen deposition is altered by silencing COMP mRNA by small interfering RNA (siRNA). Immunocytochemistry showed at 96 hours after transfection with COMP siRNA that the extracellular deposition of type I collagen was decreased compared to that observed with control siRNA. Further, COMP knockdown decreased amount collagens type I to V in the medium and on the cell surfaces. Our data suggest that COMP facilitates keloid formation by accelerating collagen deposition, thus providing a new therapeutic target.

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“…The histological reaction is the most intense around the traditional linen thread which leads to cicatrization [7]. Prolonged foreign body reaction can induce keloids and foreign body granuloma [8,9]. Absorbable suture are sometimes used in such circumstance, but the possibilities of wide scars or wound failure need to be considered.…”

Section: Discussionmentioning

confidence: 99%

Double Layer Continuous Intradermal Sutures in Keloid Operation

Long¹

2014

J Clin Exp Dermatol Res

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The Most Current Algorithms for the Treatment and Prevention of Hypertrophic Scars and Keloids

Cited by 287 publications

References 55 publications

Therapeutic potential of fibroblast growth factor-2 for hypertrophic scars: upregulation of MMP-1 and HGF expression

Therapeutic potential of fibroblast growth factor-2 for hypertrophic scars: upregulation of MMP-1 and HGF expression

Identification and Characterization of Cartilage Oligomeric Matrix Protein as a Novel Pathogenic Factor in Keloids

Double Layer Continuous Intradermal Sutures in Keloid Operation

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