| Literature DB >> 33498298 |
Paul Schilf1, Axel Künstner1,2, Michael Olbrich1, Silvio Waschina3, Beate Fuchs4, Christina E Galuska4, Anne Braun5, Kerstin Neuschütz1, Malte Seutter5, Katja Bieber1, Lars Hellberg6, Christian Sina7, Tamás Laskay6, Jan Rupp6, Ralf J Ludwig1,8, Detlef Zillikens5,8, Hauke Busch1,2,8, Christian D Sadik5,8, Misa Hirose1,8, Saleh M Ibrahim1,8,9.
Abstract
Several genetic variants in the mitochondrial genome (mtDNA), including ancient polymorphisms, are associated with chronic inflammatory conditions, but investigating the functional consequences of such mtDNA polymorphisms in humans is challenging due to the influence of many other polymorphisms in both mtDNA and the nuclear genome (nDNA). Here, using the conplastic mouse strain B6-mtFVB, we show that in mice, a maternally inherited natural mutation (m.7778G > T) in the mitochondrially encoded gene ATP synthase 8 (mt-Atp8) of complex V impacts on the cellular metabolic profile and effector functions of CD4+ T cells and induces mild changes in oxidative phosphorylation (OXPHOS) complex activities. These changes culminated in significantly lower disease susceptibility in two models of inflammatory skin disease. Our findings provide experimental evidence that a natural variation in mtDNA influences chronic inflammatory conditions through alterations in cellular metabolism and the systemic metabolic profile without causing major dysfunction in the OXPHOS system.Entities:
Keywords: ATP8; autoimmune disease; complex V; conplastic mice; immunometabolism; metabolomics; mitochondria; mt-Atp8; mtDNA polymorphisms; propionate; short chain fatty acids; skin inflammation
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Year: 2021 PMID: 33498298 PMCID: PMC7863969 DOI: 10.3390/ijms22031006
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923