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Published on: September 25, 2011
S100A8/A9 deficiency in nonhealing venous leg ulcers uncovered by multiplexed antibody microarray profiling
H Trøstrup1, R Lundquist, L H Christensen
1Copenhagen Wound Healing Center, Department of Dermatology, Bispebjerg University Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark.
The British Journal of Dermatology
|April 27, 2011
Summary
Chronic wounds show subtle molecular differences, with increased fibronectin from myofibroblasts, not excessive proteinases. This challenges current paradigms of nonhealing venous leg ulcers.
Area of Science:
- Biochemistry
- Wound Healing Research
- Proteomics
Background:
- Mechanisms of chronic nonhealing wounds remain poorly understood.
- Current knowledge of chronic wound pathogenesis is fragmented.
Purpose of the Study:
- To elucidate the pathogenesis of chronic wounds by examining protein profiles.
- To investigate the relationship between healing capacity and protein levels using a novel microarray.
Main Methods:
- Compared wound fluid from nonhealing venous leg ulcers with healing acute wounds.
- Utilized a high-throughput antibody-based microarray to measure 48 different proteins.
- Analyzed fibronectin fragmentation and levels via Western blot.
Main Results:
- No significant changes in proinflammatory cytokines, proteinases, or antiproteinases were observed.
- Matrix metalloproteinase-9 and type IV collagen levels were similar between chronic and acute wounds.
- Total fibronectin levels were doubled in chronic wounds, originating from myofibroblasts; S100A8/A9 was reduced.
Conclusions:
- Molecular anomalies in chronic wounds are more subtle than previously thought.
- Excessive proteinase activity or deficiencies in ECM proteins/growth factors do not significantly contribute to venous leg ulcer nonhealing.
- Findings suggest a revised understanding of chronic wound pathophysiology.
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