miR-200c inhibition and catalase accelerate diabetic wound healing DOI Creative Commons
M D'agostino, Sara Sileno,

Daniela Lulli

et al.

Journal of Biomedical Science, Journal Year: 2025, Volume and Issue: 32(1)

Published: Feb. 14, 2025

Abstract Background Reactive oxygen species (ROS) are increased in diabetic conditions and play a causal role foot ulcers (DFU). We previously showed that ROS up-regulate miR-200c expression, turns causes apoptosis, senescence, upregulation nitric oxide decrease, leading to endothelial disfunction. Methods The aim of this study is dissect DFU explore the potential anti-miR-200c antioxidant catalase (CAT) promoting wound healing (WH). inhibition CAT treatment were performed either immortalized keratinocytes (HaCaT) or primary fibroblasts (FBs) (KCs) deriving from patients (pts) undergoing amputations. Primary cells pts saphenectomies used as controls. blockade was via lentiviral particles bearing an sequence locked nucleic acid (LNA) oligos. Equine administered on cell medium. WH assay vivo (db/db) mice by topical with LNA wounds dissolved Pluronic gel mixture, every three days. Results found levels different stimuli known induce ROS, such ultraviolet radiation (UV), hydrogen peroxide (H 2 O ), high glucose HaCaT. also upregulated skin biopsies, FBs KCs isolated vs Forced expression induced both KCs, reduced it. improved HaCaT, under basal after UV H treatment, simultaneous accelerated pts, increasing its protein targets: sirtuin 1 (SIRT1), transcription factors FOXO1 ZEB1 decreasing p66Shc phosphorylation at Ser-36, co-treatment synergistic effects reducing cytotoxicity. Interestingly, decreased pts. Topical administration model closure. Conclusions Anti-miR-200c could be considered novel for and, possibly, other types non-diabetic ulcers.

Language: Английский

miR-200c inhibition and catalase accelerate diabetic wound healing DOI Creative Commons
M D'agostino, Sara Sileno,

Daniela Lulli

et al.

Journal of Biomedical Science, Journal Year: 2025, Volume and Issue: 32(1)

Published: Feb. 14, 2025

Abstract Background Reactive oxygen species (ROS) are increased in diabetic conditions and play a causal role foot ulcers (DFU). We previously showed that ROS up-regulate miR-200c expression, turns causes apoptosis, senescence, upregulation nitric oxide decrease, leading to endothelial disfunction. Methods The aim of this study is dissect DFU explore the potential anti-miR-200c antioxidant catalase (CAT) promoting wound healing (WH). inhibition CAT treatment were performed either immortalized keratinocytes (HaCaT) or primary fibroblasts (FBs) (KCs) deriving from patients (pts) undergoing amputations. Primary cells pts saphenectomies used as controls. blockade was via lentiviral particles bearing an sequence locked nucleic acid (LNA) oligos. Equine administered on cell medium. WH assay vivo (db/db) mice by topical with LNA wounds dissolved Pluronic gel mixture, every three days. Results found levels different stimuli known induce ROS, such ultraviolet radiation (UV), hydrogen peroxide (H 2 O ), high glucose HaCaT. also upregulated skin biopsies, FBs KCs isolated vs Forced expression induced both KCs, reduced it. improved HaCaT, under basal after UV H treatment, simultaneous accelerated pts, increasing its protein targets: sirtuin 1 (SIRT1), transcription factors FOXO1 ZEB1 decreasing p66Shc phosphorylation at Ser-36, co-treatment synergistic effects reducing cytotoxicity. Interestingly, decreased pts. Topical administration model closure. Conclusions Anti-miR-200c could be considered novel for and, possibly, other types non-diabetic ulcers.

Language: Английский

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