Loss of NNT increases expression of oxidative phosphorylation complexes in C57BL/6J hearts

Williams, Jack L., Hall, Charlotte L., Meimaridou, Eirini and Metherell, Louise A. (2021) Loss of NNT increases expression of oxidative phosphorylation complexes in C57BL/6J hearts. International Journal of Molecular Sciences, 22 (11). pp. 1-12. ISSN 1422-0067

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Official URL: https://doi.org/10.3390/ijms22116101

Abstract / Description

Nicotinamide nucleotide transhydrogenase (NNT) is a proton pump in the inner mitochondrial membrane that generates reducing equivalents in the form of NAPDH, which can be used for anabolic pathways or to remove reactive oxygen species (ROS). A number of studies have linked NNT dysfunction to cardiomyopathies and increased risk of atherosclerosis; however, biallelic mutations in humans commonly cause a phenotype of adrenal insufficiency, with rare occurrences of cardiac dysfunction and testicular tumours. Here, we compare the transcriptomes of the hearts, adrenals and testes from three mouse models: the C57BL/6N, which expresses NNT; the C57BL/6J, which lacks NNT; and a third mouse, expressing the wild-type NNT sequence on the C57BL/6J background. We saw enrichment of oxidative phosphorylation genes in the C57BL/B6J in the heart and adrenal, possibly indicative of an evolved response in this substrain to loss of Nnt. However, differential gene expression was mainly driven by mouse background with some changes seen in all three tissues, perhaps reflecting underlying genetic differences between the C57BL/B6J and -6N substrains.

Item Type: Article
Additional Information: ** From MDPI via Jisc Publications Router
Uncontrolled Keywords: C57BL/6N; C57BL/6J; NNT; RNAseq; cardiomyopathy; cellular respiration
Subjects: 500 Natural Sciences and Mathematics > 570 Life sciences; biology
600 Technology > 610 Medicine & health
Department: School of Human Sciences
SWORD Depositor: Pub Router
Depositing User: Pub Router
Date Deposited: 07 Jun 2021 11:24
Last Modified: 07 Jun 2021 11:24
URI: http://repository.londonmet.ac.uk/id/eprint/6737

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