RT info:eu-repo/semantics/article
T1 The myeloid mineralocorticoid receptor regulates dermal angiogenesis and inflammation in glucocorticoid‐induced impaired wound healing
A1 Nguyen, Van Tuan
A1 Ngo, Qui Trung
A1 Ramirez, Roberto Palacios
A1 Nakamura, Toshifumi
A1 Farman, Nicolette
A1 Aractingi, Sélim
A1 Jaisser, Frederic
AB Background and PurposeDelayed 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 ApproachSkin 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 ResultsTopical 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 ImplicationsTopical 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.
SN 0007-1188
YR 2022
FD 2022-07-21
LK https://uvadoc.uva.es/handle/10324/65929
UL https://uvadoc.uva.es/handle/10324/65929
LA spa
NO Br J Pharmacol. 2022 Dec;179(23):5222-5232
NO Producción Científica
DS UVaDOC
RD 28-nov-2024