Elevated Levels of PDGF α Receptors in Keloid Fibroblasts Contribute to an Enhanced Response to PDGF

Haisa, Minoru; Okochi, Hitoshi; Grotendorst, Gary R.

doi:10.1111/1523-1747.ep12396856

Cited by 128 publications

(95 citation statements)

References 36 publications

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“…Furthermore, we observed an induction of Fussel-15 in 2-D-cultivated fibroblasts stimulated with PDGF ( Figure 1C). Haisa et al 16 demonstrated that stimulation by PDGF enhanced cell proliferation and migration of keloid fibroblasts due to elevated levels of PDGF␣ receptors in keloid, compared with normal fibroblasts. Histological analysis of human keloid (n ϭ 4) and scleroderma (n ϭ 4) dermal tissues reveals strong Fussel-15 protein expression in both keloid and scleroderma fibroblasts (arrows), compared with fibroblasts of control dermis (n ϭ 4).…”

Section: Discussionmentioning

confidence: 99%

Fussel-15, a New Player in Wound Healing, Is Deregulated in Keloid and Localized Scleroderma

Arndt

Schmidt

Wacker

et al. 2011

The American Journal of Pathology

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Dermal wound healing depends on highly complex interplay among various cytokines and cell types. Disruption of this process can result in impaired healing in the form of excessive scarring, as is the case in fibrotic diseases such as keloid and scleroderma. In the present study, we found Fussel-15, a new member of the Ski/Sno family of TGF-␤/BMP signaling repressors, to be expressed in early wound healing and constantly overexpressed in keloid-derived and scleroderma-derived fibroblasts. Comparing the results of three-dimensional free-floating and attached-released in vitro wound healing assays, we observed that Fussel-15 is expressed during the migratory phase in the free-floating assay, indicating that Fussel-15 might play a role during fibroblast migration. Fussel-15-transfected fibroblasts showed greater migration ability in a scratch wound healing assay, compared with control-transfected cells. This migratory phenotype due to Fussel-15 was confirmed by increased peripheral F-actin localization and modifications in size, amount, and distribution of focal adhesion complexes, which were observed using F-actin and focal adhesion kinase (FAK) immunofluorescence staining, respectively. The present results suggest that expression of Fussel-15 during wound healing might promote fibroblast migration. Permanent expression of Fussel-15 in keloid and skin sclerosis fibroblasts could be involved in the pathogenesis of these conditions, but the molecular mechanism underlying this up-regulation remains to be determined.

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Section: Discussionmentioning

confidence: 99%

Fussel-15, a New Player in Wound Healing, Is Deregulated in Keloid and Localized Scleroderma

Arndt

Schmidt

Wacker

et al. 2011

The American Journal of Pathology

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“…40 In fact, there is evidence in the literature linking keloid pathogenesis with CTGF and TGF-b, which are known as potent profibrotic factors. 41,42 Further, keloid fibroblast showed an increase in the level of growth factor receptors and responded more quickly to PDGF and TGF-b as compared with normal skin fibroblasts. These growth factors could upregulate keloid fibroblasts from the start of wound healing process.…”

Section: Therapies Under Investigationmentioning

confidence: 99%

“…TGF-b2 activates p38 by Smad independent pathways that suggest the presence of positive autoregulation. 41 There has been increased interest in using botulinum toxin A as one of the treatment options to reduce scar formation through its capability to decrease the tension in the wound edges. A study conducted by Zhibo and Miaobo investigated the effect of intralesional botulinum toxin A in twelve patients in which the toxin was applied every three months for a whole period of nine months.…”

Section: Therapies Under Investigationmentioning

confidence: 99%

Novel Insights on Understanding of Keloid Scar: Article Review

Mari

Alsabri

Tabal

et al. 2015

Journal of the American College of Clinical Wound Specialists

123

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Keloid scar, dermal benign fibro-proliferative growth that extends outside the original wound and invades adjacent dermal tissue due to extensive production of extracellular matrix, especially collagen, which caused by over expression of cytokines and growth factors. Although many attempts were made to understand the exact pathophysiology and the molecular abnormalities, the pathogenesis of keloid scar is yet to be determined. Even though there are several treatment options for keloid scars include combination of medical and surgical therapies like combination of surgical removal followed by cryotherapy or intralesional steroid therapy, the reoccurrence rate is still high despite the present treatment. In this review, PubMed, clinical key and Wright State Library web site have been used to investigate any update regarding Keloid disease. We used Keloid, scar formation, hypertrophic scar and collagen as key words. More than 40 articles have been reviewed. This paper reviews literature about keloid scar formation mechanism, the most recent therapeutic options including the ones under research.

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“…pDGF is produced by platelets, macrophages, vascular endothelium, fibroblasts and keratinocytes (58,59). pDGF is released by platelets soon after injury, and recruits fibroblasts and macrophages.…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

Radiotherapy and wound healing: Principles, management and prospects (Review)

Gieringer

Gosepath²,

Naim³

2011

Oncol Rep

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Abstract. radiation therapy is a major therapeutic modality in the management of cancer patients. Over 60% of these patients receive radiotherapy at some point during their course of treatment and over 90% will develop skin reactions after therapy. problematic wound healing in radiation-damaged tissue constitutes a major surgical difficulty and despite all efforts, irradiated skin remains a therapeutic challenge. this review provides an overview of the fundamental principles of radiation therapy with regards to the wound healing in normal and irradiated skin. Furthermore, it presents techniques that describe how to prevent and manage skin side effects as well as prospects that may improve cutaneous wound repair in general and in irradiated skin.

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Elevated Levels of PDGF α Receptors in Keloid Fibroblasts Contribute to an Enhanced Response to PDGF

Cited by 128 publications

References 36 publications

Fussel-15, a New Player in Wound Healing, Is Deregulated in Keloid and Localized Scleroderma

Fussel-15, a New Player in Wound Healing, Is Deregulated in Keloid and Localized Scleroderma

Novel Insights on Understanding of Keloid Scar: Article Review

Radiotherapy and wound healing: Principles, management and prospects (Review)

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