Molecular mechanisms underlying the promotion of wound repair by coenzyme Q10: PI3K/Akt signal activation via alterations to cell membrane domains.

Autor:	Kurashiki T; Division of Biochemistry, Department of Pathophysiological and Therapeutic Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.; Division of Anesthesiology and Critical Care Medicine, Department of Surgery, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Horikoshi Y; Division of Biochemistry, Department of Pathophysiological and Therapeutic Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Kamizaki K; Division of Cell Physiology, Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, Kobe 650-0017, Japan., Sunaguchi T; Division of Biochemistry, Department of Pathophysiological and Therapeutic Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.; Division of Gastrointestinal and Pediatric Surgery, Department of Surgery, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Hara K; Division of Biochemistry, Department of Pathophysiological and Therapeutic Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.; Division of Gastrointestinal and Pediatric Surgery, Department of Surgery, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Morimoto M; Division of Gastrointestinal and Pediatric Surgery, Department of Surgery, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Kitagawa Y; Division of Anesthesiology and Critical Care Medicine, Department of Surgery, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Nakaso K; Division of Biochemistry, Department of Pathophysiological and Therapeutic Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Otsuki A; Division of Anesthesiology and Critical Care Medicine, Department of Surgery, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan., Matsura T; Division of Biochemistry, Department of Pathophysiological and Therapeutic Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Jazyk:	angličtina
Zdroj:	Journal of clinical biochemistry and nutrition [J Clin Biochem Nutr] 2022 May; Vol. 70 (3), pp. 222-230. Date of Electronic Publication: 2022 Jan 08.
DOI:	10.3164/jcbn.21-141
Abstrakt:	Coenzyme Q10 (CoQ10) promotes wound healing in vitro and in vivo . However, the molecular mechanisms underlying the promoting effects of CoQ10 on wound repair remain unknown. In the present study, we investigated the molecular mechanisms through which CoQ10 induces wound repair using a cellular wound-healing model. CoQ10 promoted wound closure in a dose-dependent manner and wound-mediated cell polarization after wounding in HaCaT cells. A comparison with other CoQ homologs, benzoquinone derivatives, and polyisoprenyl compounds suggested that the whole structure of CoQ10 is required for potent wound repair. The phosphorylation of Akt after wounding and the plasma membrane translocation of Akt were elevated in CoQ10-treated cells. The promoting effect of CoQ10 on wound repair was abrogated by co-treatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor. Immuno-histochemical and biochemical analyses showed that CoQ10 increased the localization of caveolin-1 (Cav-1) to the apical membrane domains of the cells and the Cav-1 content in the membrane-rich fractions. Depletion of Cav-1 suppressed CoQ10-mediated wound repair and PI3K/Akt signaling activation in HaCaT cells. These results indicated that CoQ10 increases the translocation of Cav-1 to the plasma membranes, activating the downstream PI3K/Akt signaling pathway, and resulting in wound closure in HaCaT cells. Competing Interests: No potential conflicts of interest were disclosed. (Copyright © 2022 JCBN.)
Databáze:	MEDLINE
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