Involvement of the mitochondrial permeability transition pore in chronic ethanol-mediated liver injury in mice

American Journal of Physiology. Gastrointestinal and Liver Physiology
Adrienne L KingShannon M Bailey

Abstract

Chronic ethanol consumption increases sensitivity of the mitochondrial permeability transition (MPT) pore induction in liver. Ca(2+) promotes MPT pore opening, and genetic ablation of cyclophilin D (CypD) increases the Ca(2+) threshold for the MPT. We used wild-type (WT) and CypD-null (CypD(-/-)) mice fed a control or an ethanol-containing diet to investigate the role of the MPT in ethanol-mediated liver injury. Ca(2+)-mediated induction of the MPT and mitochondrial respiration were measured in isolated liver mitochondria. Steatosis was present in WT and CypD(-/-) mice fed ethanol and accompanied by increased terminal deoxynucleotidyl transferase dUTP-mediated nick-end label-positive nuclei. Autophagy was increased in ethanol-fed WT mice compared with ethanol-fed CypD(-/-) mice, as reflected by an increase in the ratio of microtubule protein 1 light chain 3B II to microtubule protein 1 light chain 3B I. Higher levels of p62 were measured in CypD(-/-) than WT mice. Ethanol decreased mitochondrial respiratory control ratios and select complex activities in WT and CypD(-/-) mice. Ethanol also increased CypD protein in liver of WT mice. Mitochondria from control- and ethanol-fed WT mice were more sensitive to Ca(2+)-mediated MPT po...Continue Reading

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Citations

Jul 19, 2015·Clinics and Research in Hepatology and Gastroenterology·Lin WangXiao-Ming Yin
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Nov 25, 2020·Archives of Biochemistry and Biophysics·Fang YuanYin-Xiong Li
Jun 3, 2021·International Journal of Molecular Sciences·Agostino Di CiaulaPiero Portincasa

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