ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1997.50303.x-i3

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1994.20413.x-i1

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30105.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30101.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

摘要:

Synthesis and degradation of collagen is an essential component of wound healing. In most persons, this deposition of collagen results in the formation of a fine line scar which restores much of the tensile strength to the injured tissue and is cosmetically acceptable. However, in certain individuals, the result of wound healing is the excessive accumulation of collagen, resulting in a hypertrophic scar or keloid. The precise origin of this abnormal collagen deposition is unknown, but recent studies have begun to identify potential mechanisms for these disfiguring and painful lesions. This article will review the clinical and laboratory findings pertinent to understanding the origin and treatment of excessive scarring.

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30106.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30102.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

摘要:

This case report concerns an individual with a defect in wound healing which resulted in recurring, bilateral pneumothoraces during the late postoperative period. This patient had no history of systemic disease or wound healing abnormalities before his recurrent wound disruption. Physical examination and routine biochemical studies failed to identify any causative agent for the multiple wound dehiscences in the patient. Histologic examination of scar tissue showed collagen fiber bundles with a diameter 50% less than that of normal fibrils. Elastic fibers were barely visible, and the scar tissue included a large number of inflammatory cells. A significant finding was an elevated and aberrant expression of collagenase by a fibroblast cell line established from a skin biopsy specimen. This enhanced level of collagenase expression could be inhibited by treatment of the cells with diphenylhydantoin, an inhibitor of collagenase biosynthesis. After initiation of diphenylhydantoin therapy, the patient's scar formation normalized with the recurrent pneumothoraces. These findings support the conclusion that an abnormal expression of collagenase resulted in enhanced degradation of collagen in the patient's wounds, thereby leading to wound dehiscence.

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30107.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

摘要:

To investigate the role of transforming growth factor‐β1in tissue repair, we performed wound healing studies in the transforming growth factor‐β1—deficient mouse with targeted disruption of the transforming growth factor‐β1gene. Transforming growth factor‐β1—deficient mice exhibit no obvious developmental defects and are phenotypically normal until approximately 3 weeks of age when a severe wasting syndrome develops, accompanied by an overwhelming inflammatory response resulting in multisystem organ failure and death. Full‐thickness 0.5 × 0.5 cm skin wounds were created on the backs of 10‐day‐old mice (wild type or heterozygous controls versus homozygous transforming growth factor‐β1—deficient mutants) and covered with a nonabsorbent dressing (OpSite). Serial wound measurements were made, and percentage of wound closure over time was determined. On day 10, wounds and liver were harvested for histologic and molecular analysis. Histologic scores were assigned (1 [no healing] to 12 [complete healing]) on the basis of granulation tissue formation, vascularity, collagen deposition, and epithelialization. Reverse transcription—polymerase chain reaction was performed to detect messenger RNA transcripts for transforming growth factor‐β1, transforming growth factor‐β2, platelet‐derived growth factor A‐chain and B‐chain, interleukin‐1β and ‐6, and tumor necrosis factor‐α in unwounded skin, day 10 wounds, and liver. No significant differences in wound closure were observed until day 10. Weight gain, however, was significantly decreased in the mutant animals as early as day 6. Histologic scores were significantly lower in the transforming growth factor‐β1—deficient mutants (5.4 ± 0.6 versus 11.1 ± 0.3,p<0.01, Wilcoxon rank‐sum test) and showed decreased granulation tissue formation, vascularity, collagen deposition, and epithelialization and a marked inflammatory infiltrate. As expected, transforming growth factor‐β1was expressed in controls but not mutants. Transforming growth factor‐β2, platelet‐derived growth factor A‐chain and B‐chain, and tumor necrosis factor‐α were constitutively expressed in unwounded skin, day 10 wounds, and liver of both controls and mutants. Interleukin‐1β and ‐6, however, were induced after wounding. Early wound healing in the transforming growth factor‐β1—deficient mouse proceeds relatively normally because of upregulation or functional redundancy of other growth factors or possibly because of maternal rescue by means of transforming growth factor‐β1transmitted in milk. Loss of transforming growth factor‐β1regulation ultimately results in a marked inflammatory response, as evidenced by the histologic appearance of the wound and increased expression of the inflammatory cytokines (tumor necrosis factor‐α, interleukin‐1β and 6). The sev

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30108.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

摘要:

Tenascin is an extracellular matrix molecule with structural similarity to fibronectin. An increase in extracellular matrix content of both tenascin and fibronectin is associated with early wound healing and with various skin fibroses. However, the relationship of tenascin and fibronectin expression during scar remodeling and the formation of pathologic scars such as keloids is unknown. Expression of tenascin in normal and abnormal human scars was examined and compared with that of fibronectin by immunohistochemistry and in situ hybridization. Tenascin and fibronectin protein and messenger RNA contents were elevated in normal, mature scars relative to quiescent skin, similar to the situation during earlier stages of healing. Tenascin and fibronectin expression was further enhanced in keloids relative to normal skin and scar, and, as has been shown for fibronectin, tenascin expression in uninjured skin adjacent to keloids was indistinguishable from that in quiescent skin from unaffected individuals. These data suggest that tenascin and fibronectin gene expression are coordinated during later stages of normal wound healing and that a defect involving common regulatory elements for these genes is associated with the formation of keloids.

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30109.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY

摘要:

Interleukin‐4 increases the synthesis of extracellular matrix proteins, including types I and III collagen and fibronectin, by both human and rat fibroblasts. Because fibroblasts are the final common effector cells of most phases of tissue repair, this study set out to investigate the effects of interleukin‐4 on the healing of three different types of wounds. Acute excisional and chronic granulating wounds inoculated withEscherichia coliand incisional wounds in streptozotocin‐induced diabetic Sprague‐Dawley rats were used. Recombinant murine or human interleukin‐4 was applied topically to the open wounds at doses of 0.1, 1.0, or 10.0 µg/cm2/wound for 5 or 10 days. Incisional wounds received the same doses once—at the time of wounding. The time taken to achieve wound closure or wound breaking strength measurements of wounds was recorded and compared with relevant untreated control groups. Wound contraction was impaired in the presence of bacteria, and this was reversed by all doses of recombinant murine interleukin‐4. Recombinant murine interleukin‐4 had no effect on the wound closure of noncontaminated wounds; it reduced wound breaking strength in acute excisional wounds, except in a contaminated setting when wounds were treated with 1.0 pg/cm2/wound. Recombinant interleukin‐4 (1.0 µg) improved breaking strength of both diabetic and normal incisional wounds. The apparent pleiotropic effect of interleukin‐4 on wound breaking strength under different wound conditions may be related not only to the activity of the fibroblast but also the ratio of cross‐linked collagen/total collagen content of wounds. This study suggests that interleukin‐4 may be a useful agent for accelerating closure of wounds, particularly

ISSN:1067-1927    

DOI:10.1046/j.1524-475X.1995.30110.x

出版商:Blackwell Science    

年代:1995

数据来源: WILEY