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  1. AU="Ketomäki, Tuomo"
  2. AU=Cavallini Giorgio
  3. AU="Saha, Aakash"
  4. AU="Noguchi, J"
  5. AU="Löhr, B."
  6. AU="Lokie, Kelsey B"

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  1. Artikel ; Online: Author Correction: Systemically administered wound-homing peptide accelerates wound healing by modulating syndecan-4 function.

    Maldonado, Horacio / Savage, Bryan D / Barker, Harlan R / May, Ulrike / Vähätupa, Maria / Badiani, Rahul K / Wolanska, Katarzyna I / Turner, Craig M J / Pemmari, Toini / Ketomäki, Tuomo / Prince, Stuart / Humphries, Martin J / Ruoslahti, Erkki / Morgan, Mark R / Järvinen, Tero A H

    Nature communications

    2024  Band 15, Heft 1, Seite(n) 234

    Sprache Englisch
    Erscheinungsdatum 2024-01-03
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-44574-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Systemically administered wound-homing peptide accelerates wound healing by modulating syndecan-4 function.

    Maldonado, Horacio / Savage, Bryan D / Barker, Harlan R / May, Ulrike / Vähätupa, Maria / Badiani, Rahul K / Wolanska, Katarzyna I / Turner, Craig M J / Pemmari, Toini / Ketomäki, Tuomo / Prince, Stuart / Humphries, Martin J / Ruoslahti, Erkki / Morgan, Mark R / Järvinen, Tero A H

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 8069

    Abstract: CAR (CARSKNKDC) is a wound-homing peptide that recognises angiogenic neovessels. Here we discover that systemically administered CAR peptide has inherent ability to promote wound healing: wounds close and re-epithelialise faster in CAR-treated male mice. ...

    Abstract CAR (CARSKNKDC) is a wound-homing peptide that recognises angiogenic neovessels. Here we discover that systemically administered CAR peptide has inherent ability to promote wound healing: wounds close and re-epithelialise faster in CAR-treated male mice. CAR promotes keratinocyte migration in vitro. The heparan sulfate proteoglycan syndecan-4 regulates cell migration and is crucial for wound healing. We report that syndecan-4 expression is restricted to epidermis and blood vessels in mice skin wounds. Syndecan-4 regulates binding and internalisation of CAR peptide and CAR-mediated cytoskeletal remodelling. CAR induces syndecan-4-dependent activation of the small GTPase ARF6, via the guanine nucleotide exchange factor cytohesin-2, and promotes syndecan-4-, ARF6- and Cytohesin-2-mediated keratinocyte migration. Finally, we show that genetic ablation of syndecan-4 in male mice eliminates CAR-induced wound re-epithelialisation following systemic administration. We propose that CAR peptide activates syndecan-4 functions to selectively promote re-epithelialisation. Thus, CAR peptide provides a therapeutic approach to enhance wound healing in mice; systemic, yet target organ- and cell-specific.
    Mesh-Begriff(e) Male ; Mice ; Animals ; Syndecan-4/genetics ; Syndecan-4/metabolism ; Wound Healing/physiology ; Peptides/metabolism ; Epidermis/metabolism ; Epidermal Cells/metabolism ; Cell Movement
    Chemische Substanzen Syndecan-4 ; Peptides
    Sprache Englisch
    Erscheinungsdatum 2023-12-06
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-43848-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: R-Ras regulates vascular permeability, but not overall healing in skin wounds.

    Ketomäki, Tuomo / Vähätupa, Maria / May, Ulrike / Pemmari, Toini / Ruikka, Ella / Hietamo, Jussi / Kaipiainen, Pirkka / Barker, Harlan / Parkkila, Seppo / Uusitalo-Järvinen, Hannele / Järvinen, Tero A H

    Experimental dermatology

    2018  Band 28, Heft 2, Seite(n) 202–206

    Abstract: Wounds close by keratinocytes migrating from the edge of the wound and re-epithelializing the epidermis. It has been proposed that the major stimuli for wound closure are blood-derived growth factors, chemokines and cytokines. The small GTPase R-Ras, a ... ...

    Abstract Wounds close by keratinocytes migrating from the edge of the wound and re-epithelializing the epidermis. It has been proposed that the major stimuli for wound closure are blood-derived growth factors, chemokines and cytokines. The small GTPase R-Ras, a known integrin activator, also regulates vascular permeability during angiogenesis, and blood vessels lacking R-Ras leak plasma proteins constantly. We explored whether the access to blood-derived proteins influences skin wound healing in R-Ras knockout (KO) mice. In skin wounds, R-Ras expression was mostly restricted to the vasculature in the granulation tissue. Angiogenic blood vessels in the R-Ras KO mice were significantly more permeable than in wild-type (WT) controls. Although the distances between epidermal tongues, and the panniculus carnosus muscles, were significantly longer in R-Ras KO than WT controls before the granulation tissue formation took place, there were no differences in the wound closure or re-epithelialization rates or granulation tissue formation. These findings were also corroborated in a special splint excision wound model. Our study shows that although R-Ras does not influence the skin wound healing itself, the blood vessels lacking R-Ras are leaky and thus could facilitate the access of blood-derived proteins to the wound.
    Mesh-Begriff(e) Animals ; Capillary Permeability ; Cell Movement ; Epidermis/metabolism ; Female ; Guanosine Triphosphate/chemistry ; Integrins/metabolism ; Keratinocytes/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microcirculation ; Neovascularization, Pathologic ; Re-Epithelialization ; Skin/metabolism ; Skin Diseases/metabolism ; Wound Healing ; ras Proteins/genetics ; ras Proteins/metabolism
    Chemische Substanzen Integrins ; Guanosine Triphosphate (86-01-1) ; Rras protein, mouse (EC 3.6.1.-) ; ras Proteins (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2018-12-21
    Erscheinungsland Denmark
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1130936-2
    ISSN 1600-0625 ; 0906-6705
    ISSN (online) 1600-0625
    ISSN 0906-6705
    DOI 10.1111/exd.13851
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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