Protective and healing effects of apoptotic mimic-induced M2-like macrophage polarization on pressure ulcers in young and middle-aged mice

Riki Toita, Eiko Shimizu, Masaharu Murata, Jeong Hun Kang

研究成果: Contribution to journalArticle査読

2 被引用数 (Scopus)

抄録

Pressure ulcers (PUs) have no cure and are of significant health and economic concern worldwide, owing to the increasing population of elderly individuals at high risk for PU and who have impaired tissue repair. Macrophages play a pivotal role in PU development and healing. Imbalances between M1 (inflammatory) and M2 (anti-inflammatory/reparative) macrophages result in delayed resolution of inflammation and wound healing. We hypothesized that M1-to-M2 macrophage polarization mediated by artificial apoptotic cell mimics, phosphatidylserine-containing liposomes (PSLs), would protect against PU formation and accelerate PU healing in young (2-month-old) and middle-aged (12-month-old) mice. We used a clinically relevant murine model of ischemia-reperfusion-induced PU. Middle-aged mice displayed the delayed wound healing associated with increased inflammation, decreased collagen deposition, reduced angiogenesis, and delayed wound closure relative to their younger counterparts. PSL treatment significantly inhibited PU formation and promoted tissue remodeling in both age groups. These effects were mediated by increased M1-to-M2 macrophage polarization, induced by the PSLs. Thus, this study suggests, for the first time, that PSL-induced M2-like macrophage polarization is a promising strategy to protect against PU formation and promote PU repair in human patients of all ages.

本文言語英語
ページ(範囲)705-714
ページ数10
ジャーナルJournal of Controlled Release
330
DOI
出版ステータス出版済み - 2 10 2021

All Science Journal Classification (ASJC) codes

  • 薬科学

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