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dc.contributor.authorYannas, Ioannis V
dc.contributor.authorTzeranis, Dimitrios
dc.contributor.authorSo, Peter T. C.
dc.date.accessioned2019-02-04T20:45:21Z
dc.date.available2019-02-04T20:45:21Z
dc.date.issued2017-03
dc.identifier.issn1067-1927
dc.identifier.urihttp://hdl.handle.net/1721.1/120183
dc.description.abstractWe review the mounting evidence that regeneration is induced in wounds in skin and peripheral nerves by a simple modification of the wound healing process. Here, the process of induced regeneration is compared to the other two well-known processes by which wounds close, i.e., contraction and scar formation. Direct evidence supports the hypothesis that the mechanical force of contraction (planar in skin wounds, circumferential in nerve wounds) is the driver guiding the orientation of assemblies of myofibroblasts (MFB) and collagen fibers during scar formation in untreated wounds. We conclude that scar formation depends critically on wound contraction and is, therefore, a healing process secondary to contraction. Wound contraction and regeneration did not coincide during healing in a number of experimental models of spontaneous (untreated) regeneration described in the literature. Furthermore, in other studies in which an efficient contraction-blocker, a collagen scaffold named dermis regeneration template (DRT), and variants of it, were grafted on skin wounds or peripheral nerve wounds, regeneration was systematically observed in the absence of contraction. We conclude that contraction and regeneration are mutually antagonistic processes. A dramatic change in the phenotype of MFB was observed when the contraction-blocking scaffold DRT was used to treat wounds in skin and peripheral nerves. The phenotype change was directly observed as drastic reduction in MFB density, dispersion of MFB assemblies and loss of alignment of the long MFB axes. These observations were explained by the evidence of a surface-biological interaction of MFB with the scaffold, specifically involving binding of MFB integrins α[subscript 1]β[subscript 1] and α[subscript 2]β[subscript 1] to ligands GFOGER and GLOGER naturally present on the surface of the collagen scaffold. In summary, we show that regeneration of wounded skin and peripheral nerves in the adult mammal can be induced simply by appropriate control of wound contraction, rather than of scar formation.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant RO1 NS051320)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant 5‐P41‐EB015871‐28)en_US
dc.description.sponsorshipHorizon 2020 Framework Programme (European Commission) (Grant DLV‐658850)en_US
dc.description.sponsorshipSingapore-MIT Alliance for Research and Technology (SMART) (Grant 5‐P41‐EB015871‐28)en_US
dc.description.sponsorshipHamamatsu Corporationen_US
dc.publisherWileyen_US
dc.relation.isversionofhttp://dx.doi.org/10.1111/WRR.12516en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alikeen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/en_US
dc.sourcePMCen_US
dc.titleRegeneration of injured skin and peripheral nerves requires control of wound contraction, not scar formationen_US
dc.typeArticleen_US
dc.identifier.citationYannas, Ioannis V., Dimitrios S. Tzeranis, and Peter T. C. So. “Regeneration of Injured Skin and Peripheral Nerves Requires Control of Wound Contraction, Not Scar Formation.” Wound Repair and Regeneration 25, no. 2 (April 2017): 177–191.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Mechanical Engineeringen_US
dc.contributor.mitauthorYannas, Ioannis V
dc.contributor.mitauthorTzeranis, Dimitrios
dc.contributor.mitauthorSo, Peter T. C.
dc.relation.journalWound Repair and Regenerationen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2019-01-04T13:38:33Z
dspace.orderedauthorsYannas, Ioannis V.; Tzeranis, Dimitrios S.; So, Peter T. C.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0003-0151-708X
dc.identifier.orcidhttps://orcid.org/0000-0003-4698-6488
mit.licenseOPEN_ACCESS_POLICYen_US


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