Hv1-deficiency protects ß cells from glucotoxicity through regulation of NOX4 level.
Biochem Biophys Res Commun
; 513(2): 434-438, 2019 05 28.
Article
em En
| MEDLINE
| ID: mdl-30967259
ABSTRACT
High glucose (HG)-induced oxidative stress contributes to the dysfunction of pancreatic ß cells in diabetes. The voltage-gated proton channel Hv1 has been proposed to support reactive oxygen species (ROS) production during respiratory bursts. However, the effect of Hv1 on glucotoxicity in pancreatic ß cells is not clear yet. In this study, we examined the protective effects of Hv1-deficiency in HG cultured ß cells. Following 48â¯h of treatment with 30â¯mM high glucose, Hv1 KO ß cells showed higher cell viability, lower cell apoptosis and a more stable insulin gene expression level compared to WT ß cells. In both control and HG cultured ß cells, deficiency of Hv1 decreased the glucose- and PMA-induced ROS production. Finally, HG incubation led to NOX4 upregulation in WT ß cells, which could be inhibited by HV1 deficiency. In conclusion, Hv1-deficiency prevents the HG treatment-induced NOX4 upregulation and protects ß cells from glucotoxicity.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estresse Oxidativo
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Células Secretoras de Insulina
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NADPH Oxidase 4
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Hiperglicemia
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Canais Iônicos
Limite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2019
Tipo de documento:
Article