The Role Of MMPs In Chronic Wound Edema

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Factors that are known to activate matrix  metalloproteinase (MMP) expression include growth factors (GF), tumor necrosis factor (TNF), interleukin-1 (IL-1), interlukin-6, interlukin-8 and various cellular interactions. Keratinocytes, fibroblasts, macroph
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Author(s): 
By Adrianne P.S. Smith, MD, FACEP

References
1. Vu TH, Werb Z. “Matrix metalloproteinases: effectors of development and normal physiology.” Genes and Development. Vol. 14, No. 17, pp. 2123-2133, Sep 1, 2000.
2. Cullen B. “Part 2: The Role of Oxidized Regenerated Cellulose/Collagen in Chronic Wound Repair” in Matrix Metalloprotease Modulation and Growth Factor Protection. http://www.podiatrytoday.com/WNDS/matrix/pt.cfm.
3. Stacey, Woosey, Wallace. “The Influence of Micro-Environment And Cell Phenotype On Venous Ulcer Healing.” Abstract. European Tissue Repair Society (ETRS). Annual Conference 2001. http://www.etrs.org/bulletin8_3/page7b.html.
4. Rogers, Jude, Oyibo. “Matrix Metalloproteinase (MMP) And Tissue Inhibitor Of Metalloproteinase (TIMP) Expression In Diabetic And Venous Ulcers.” Abstract. European Tissue Repair Society (ETRS). Annual Conference 2001. http://www.etrs.org/bulletin8_3/page7b.html.
5. Ergul et.al. “Evidence for a matrix metalloproteinase Induction/activation system in arterial vasculature and decreased synthesis and activity in diabetes”. American Diabetes Association, Oct 2002. http://www.heart1.com/news/newsfeed.cfm/1280/1.
6. Renò, et. al “Release and Activation of Matrix Metalloproteinase-9 During In Vitro Mechanical Compression in Hypertrophic Scars”. Arch Dermatol. 2002;138:475-478
http://archderm.ama-assn.org/issues/v138n4/abs/dst00137.html
7. Cook, et al., J Invest Dermatol 2000; 115: 225–233.
8. Herouy Y, et. al., “Lipodermatosclerosis is characterized by elevated expression and activation of matrix metalloproteinase: Implications for venous ulcer formation: J Invest Dermatol 1988; 111:822-27.
9. Abstract and commentary by: Fedor Lurie, MD, PhD. Volume 8, Number 12 www.venousdigest.com December 2001.

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Anonymoussays: June 8, 2009 at 1:52 am

Thanks a lot for publishing the above article. We surprisingly observed a unique effect on chronic wound healing as diabetic non healing ones. The events we observed were as clot formation(fibrin deposites - hemostatic phase) followed by autodebridementation of necrotic lesions compressing rejection of necrotic tisuues from the periphery to the central wound associated with ECM deposit( inflammation phase)follwoed by granulation tissue formation and wound size decrease (proliferation phase) and complete wound healing in a physiological timed manner. The cases were involved with non healing wound types of diabetes related awith and without hemodyalised states and resistant to therapy of more than 10 months up to 20 months. Our group is ready to exchange experiments and introduce our patent remedy as needed. We welcome all aspects of collaboration in mass production and research projects.
Khodaberdi Kalavi Iran, Mobile: 9111773982, Tel(home): +98 171 3351080, fax: +98 171 4423630, 2269210 Email: kalavi25@yahoo.com. kalavi@goums.ac.ir

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Anonymoussays: March 27, 2010 at 11:47 pm excellent idea on wound healing Reply to this comment »

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