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  • 1
    Electronic Resource
    Electronic Resource
    Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 11 (2003), S. 0 
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Hypertrophic scars result from excessive collagen deposition at sights of healing dermal wounds and can be functionally and cosmetically problematic. Pharmacological regulation of collagen synthesis and deposition is a direct approach to the control of scar tissue formation. We tested the ability of the phenanthrolinone derivative FG-1648 (in 0.5% Carbopol 971 PNF gel, pH 6.5), a prolyl 4-hydroxylase inhibitor, to reduce hypertrophic scar formation in a rabbit ear hypertrophic scar model. New Zealand White rabbits were divided into two treatment groups (n = 12 wounds per group with an equal number of controls): low-dose group: 0.5% FG-1648; high-dose group: 1% FG-1648. Left ears were used for treatment and right ear for control. Four 7-mm dermal ulcer wounds were made on each ear. The inhibitor was topically applied to the wound at the time of wounding and once daily up to postoperative day 7. Wounds were harvested at postoperative day 28 and scar hypertrophy quantified by measurement of the scar elevation index. All wounds showed complete healing. Treatment of wounds with 1% prolyl 4-hydroxylase inhibitor decreased the scar elevation index by 26% compared to control wounds (p 〈 0.01). Wounds treated with 0.5% FG-1648 inhibitor showed no difference in scar elevation compared to control wounds. These results suggest that inhibition of prolyl 4-hydroxylase may be a suitable agent for topical treatment for the prevention of hypertrophic scar tissue. (WOUND REP REG 2003;11:368–372)
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd.
    Wound repair and regeneration 9 (2001), S. 0 
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In vitro, transforming growth factor-α is an important factor controlling epithelial cell proliferation and migration. However, the transforming growth factor-α knockout mouse has shown no wound epithelialization defect in tail amputation and full-thickness back wounds. To resolve this disparity, we combined a full-thickness head wound and a partial-thickness ear wound on the transforming growth factor-α knockout mouse for analysis of wound epithelialization with or without granulation tissue formation. Three-millimeter ear wounds were made on the transforming growth factor-α knockout and heterozygous control mice. Full-thickness head wounds were made using a 6-mm trephine on the crown of the skull. In the ear model, transforming growth factor-α knockout mice had significantly larger epithelial gaps versus control at post-operative day 3 and 5. Epithelial thickness at the wound edge of transforming growth factor-α deficient mice was also depressed at post-operative day 3 and post-operative day 5 compared to control mice. On post-operative day 8, most wounds of both groups were epithelialized. In contrast, no difference in epithelial gap or new granulation tissue was found in the head model. The data support the concept that transforming growth factor-α plays a significant early role in wound epithelialization in vivo but its deficit is compensated if accompanied by granulation tissue formation. The data further show the importance of appropriate wound models to address the role of vulnerary factors.
    Type of Medium: Electronic Resource
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