A novel target for the promotion of dermal wound healing: Ryanodine receptors.
Toxicol Appl Pharmacol
; 366: 17-24, 2019 03 01.
Article
em En
| MEDLINE
| ID: mdl-30684528
ABSTRACT
Ryanodine receptors have an important role in the regulation of intracellular calcium levels in the nervous system and muscle. It has been described that ryanodine receptors influence keratinocyte differentiation and barrier homeostasis. Our goal was to examine the role of ryanodine receptors in the healing of full-thickness dermal wounds by means of in vitro and in vivo methods. The effect of ryanodine receptors on wound healing, microcirculation and inflammation was assessed in an in vivo mouse wound healing model, using skin fold chambers in the dorsal region, and in HaCaT cell scratch wound assay in vitro. SKH-1 mice were subjected to sterile saline (nâ¯=â¯36) or ryanodine receptor agonist 4-chloro-m-cresol (0.5â¯mM) (nâ¯=â¯42) or ryanodine receptor antagonist dantrolene (100⯵M) (nâ¯=â¯42). Application of ryanodine receptor agonist 4-chloro-m-cresol did not influence the studied parameters significantly, whereas ryanodine receptor antagonist dantrolene accelerated the wound closure. Inhibition of the calcium channel also increased the vessel diameters in the wound edges during the process of healing and increased the blood flow in the capillaries at all times of measurement. Furthermore, application of dantrolene decreased xanthine-oxidoreductase activity during the inflammatory phase of wound healing. Inhibition of ryanodine receptor-mediated effects positively influence wound healing. Thus, dantrolene may be of therapeutic potential in the treatment of wounds.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Pele
/
Cicatrização
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Ferimentos Penetrantes
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Bloqueadores dos Canais de Cálcio
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Queratinócitos
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Canal de Liberação de Cálcio do Receptor de Rianodina
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Dantroleno
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Humans
/
Male
Idioma:
En
Revista:
Toxicol Appl Pharmacol
Ano de publicação:
2019
Tipo de documento:
Article