Recombinant human decorin inhibits TGF-β1-induced contraction of collagen lattice by hypertrophic scar fibroblasts

Zhang, Zhi; Garrón, Tania; Li, Xiaojian; Liu, Yan; Zhang, Xiong; Li, Yeyang; Xu, Wenteng

doi:10.1016/j.burns.2008.08.021

Cited by 73 publications

(52 citation statements)

References 44 publications

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“…The low levels of decorin found in hypertrophic scarring may thus account for their irregular collagen organization, as well as increased ECM production (77). Zhang and colleagues (78) showed similar results, with decorin inhibiting both the basal and TGF-β1-enhanced contraction of collagen gel by both normal and hypertrophic scar fibroblasts, suggesting that decorin may have therapeutic potential for excessive skin contraction as observed in hypertrophic scarring. Mukhopadhyay and colleagues (79) examined the role of decorin in keloid tissue and found that decorin was able to decrease extracellular matrix proteins, highlighting its importance as an antifibrotic agent.…”

Section: Matrix Remodeling/maturation Phasementioning

confidence: 77%

Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies

Gauglitz

Körting

Pavicic

et al. 2010

Mol Med

1,148

1,012

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Excessive scars form as a result of aberrations of physiologic wound healing and may arise following any insult to the deep dermis. By causing pain, pruritus and contractures, excessive scarring significantly affects the patient's quality of life, both physically and psychologically. Multiple studies on hypertrophic scar and keloid formation have been conducted for decades and have led to a plethora of therapeutic strategies to prevent or attenuate excessive scar formation. However, most therapeutic approaches remain clinically unsatisfactory, most likely owing to poor understanding of the complex mechanisms underlying the processes of scarring and wound contraction. In this review we summarize the current understanding of the pathophysiology underlying keloid and hypertrophic scar formation and discuss established treatments and novel therapeutic strategies.

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Section: Matrix Remodeling/maturation Phasementioning

confidence: 77%

Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies

Gauglitz

Körting

Pavicic

et al. 2010

Mol Med

1,148

1,012

View full text Add to dashboard Cite

show abstract

“…Moreover, they generate the mechanical force that initiates wound contraction [10], which contributes to wound healing by decreasing the wound area and forming a scar [11]. However, undesirable wound contraction can lead to cosmetic and functional problems [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…TGF-β1 plays a vital role in the pathogenesis of hypertrophic scar formation [11,17]. Hypertrophic scar fibroblasts produce more TGF-β1 protein and mRNA than do normal dermal fibroblasts [2,11].…”

Section: Discussionmentioning

confidence: 99%

Differences in Hypertrophic Scar Fibroblasts according to Scar Severity: Expression of Transforming Growth Factor β1 at the mRNA and Protein Levels

Kim

Nam

Park

et al. 2015

Arch Aesthetic Plast Surg

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“…Three distinct steps of fibrillogenesis during tendon development have been described: (1) immature fibril assembly (corresponding to days 12-16 of chick embryonic metatarsal tendon development); (2) linear growth (days 16 and 17); and (3) lateral growth (days 17 and 18) (Birk et al, 1995;Zhang et al, 2005). Collagen type III and decorin have been shown to be involved in the regulation of collagen fibrillogenesis (Vogel et al, 1984;Thieszen and Rosenquist, 1995;Danielson et al, 1997;Hakkinen et al, 2000;Zhang et al, 2006). Collagen type III is a member of the fibrillar collagen family and the second most abundant collagen molecule in tendon.…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal protein distribution of TGF‐βs, their receptors, and extracellular matrix molecules during embryonic tendon development

Kuo

Petersen

Tuan

2008

Developmental Dynamics

109

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Tendon is one of the least understood tissues of the musculoskeletal system in terms of development and morphogenesis. Collagen fibrillogenesis has been the most studied aspect of tendon development, focusing largely on the role of matrix molecules such as collagen type III and decorin. While involvement of matrix molecules in collagen fibrillogenesis during chick tendon development is well understood, the role of growth factors has yet to be elucidated. This work examines the expression patterns of transforming growth factor (TGF) -␤1, -␤2, and -␤3, and their receptors with respect to expression patterns of collagen type III, decorin, and fibronectin. We focus on the intermediate stages of tendon development in the chick embryo, a period during which the tendon micro-and macro-architecture are being established. Our findings demonstrate for the first time that TGF-␤1, -␤2, and -␤3 have distinct spatiotemporal developmental protein localization patterns in the developing tendon and strongly suggest that these isoforms have independent roles in tendon development.

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Recombinant human decorin inhibits TGF-β1-induced contraction of collagen lattice by hypertrophic scar fibroblasts

Cited by 73 publications

References 44 publications

Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies

Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies

Differences in Hypertrophic Scar Fibroblasts according to Scar Severity: Expression of Transforming Growth Factor β1 at the mRNA and Protein Levels

Spatiotemporal protein distribution of TGF‐βs, their receptors, and extracellular matrix molecules during embryonic tendon development

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