A recent study by Dr. Erkki Ruoslahti published in PNAS, using a wound-homing peptide, CARSKNKDC, to tag decorin, in vivo, showed that the peptide-tagged decorin significantly reduced scar formation in mice.
Proc Natl Acad Sci U S A. 2010 Nov 24. [Epub ahead of print]
Target-seeking antifibrotic compound enhances wound healing and suppresses scar formation in mice.
Järvinen TA, Ruoslahti E.
Vascular Mapping Laboratory, Center for Nanomedicine, Sanford-Burnham Medical Research Institute, University of California, Santa Barbara, CA 93106 and Cancer Research Center, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037.
Abstract
Permanent scars form upon healing of tissue injuries such as those caused by ischemia (myocardial infarction, stroke), trauma, surgery, and inflammation. Current options in reducing scar formation are limited to local intervention. We have designed a systemically administered, target-seeking biotherapeutic for scar prevention. It consists of a vascular targeting peptide that specifically recognizes angiogenic blood vessels and extravasates into sites of injury, fused with a therapeutic molecule, decorin. Decorin prevents tissue fibrosis and promotes tissue regeneration by inhibiting TGF-β activity and by other regulatory activities. The decorin-targeting peptide fusion protein had substantially increased neutralizing activity against TGF-β1 in vitro compared with untargeted decorin. In vivo, the fusion protein selectively accumulated in wounds, and promoted wound healing and suppressed scar formation at doses where nontargeted decorin was inactive. These results show that selective targeting yields a tissue-healing and scar-reducing compound with enhanced specificity and potency. This approach may help make reducing scar formation by systemic drug delivery a feasible option for surgery and for the treatment of pathological processes in which scar formation is a problem.
PMID: 21106754 [PubMed - as supplied by publisher]
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