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    •   UVaDOC Startseite
    • WISSENSCHAFTLICHE ARBEITEN
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    • Dpto. Bioquímica y Biología Molecular y Fisiología
    • DEP06 - Artículos de revista
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    Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/65929

    Título
    The myeloid mineralocorticoid receptor regulates dermal angiogenesis and inflammation in glucocorticoid‐induced impaired wound healing
    Autor
    Nguyen, Van Tuan
    Ngo, Qui Trung
    Palacios Ramírez, RobertoAutoridad UVA Orcid
    Nakamura, Toshifumi
    Farman, Nicolette
    Aractingi, Sélim
    Jaisser, Frederic
    Año del Documento
    2022-07-21
    Descripción
    Producción Científica
    Documento Fuente
    Br J Pharmacol. 2022 Dec;179(23):5222-5232
    Zusammenfassung
    Background and Purpose Delayed wound healing is among the deleterious consequences of over-activation of the mineralocorticoid receptor (MR) induced by topical dermocorticoids. The role of dermal inflammation and angiogenesis in the benefits of MR blockade is unknown. Experimental Approach Skin wounds were made on C57Bl6 mice after topical pretreatment with the dermocorticoid clobetasol. The impact of topical MR blockade by canrenoate on inflammation, angiogenesis, and the wound macrophage phenotype was analysed 5 days post-wounding. Similar experiments were conducted on mice with genetic deletion of the MR in myeloid cells. Key Results Topical inhibition of the MR with canrenoate improved delayed wound healing through the resolution of prolonged inflammation in glucocorticoid-pretreated mouse skin. This effect was associated with a higher ratio of anti-inflammatory macrophages versus pro-inflammatory macrophages in wounds treated by canrenoate. Furthermore, MR blockade led to upregulated expression of pro-angiogenic factors and improved impaired angiogenesis in wounds of glucocorticoid-pretreated skin. Finally, deletion of MR expression by myeloid cells reproduced the benefits of topical pharmacological MR blockade. Conclusion and Implications Topical MR antagonism facilitates the switching of macrophages towards an anti-inflammatory phenotype, which improves prolonged inflammation and induces angiogenesis to accelerate wound healing delayed by glucocorticoid treatment.
    ISSN
    0007-1188
    Revisión por pares
    SI
    DOI
    10.1111/bph.15932
    Version del Editor
    https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.15932
    Idioma
    spa
    URI
    https://uvadoc.uva.es/handle/10324/65929
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
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    • DEP06 - Artículos de revista [353]
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    4.- BPH-179-5222-1.pdf
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