Defective COX1 expression in aging mice liver

Author:

Witte Steffen1,Boshnakovska Angela1,Özdemir Metin1,Chowdhury Arpita1,Rehling Peter1234ORCID,Aich Abhishek12

Affiliation:

1. University Medical Center 1 Department of Cellular Biochemistry , , Göttingen, 37073 , Germany

2. Cluster of Excellence “Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells” (MBExC), University of Göttingen 2 , Göttingen, 37075 , Germany

3. Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Translational Neuroinflammation and Automated Microscopy 3 , Göttingen, 37075 , Germany

4. Max Planck Institute for Multidisciplinary Sciences 4 , Göttingen, 37077 , Germany

Abstract

ABSTRACT Mitochondrial defects are associated with aging processes and age-related diseases, including cardiovascular diseases, neurodegenerative diseases and cancer. In addition, some recent studies suggest mild mitochondrial dysfunctions appear to be associated with longer lifespans. In this context, liver tissue is considered to be largely resilient to aging and mitochondrial dysfunction. Yet, in recent years studies report dysregulation of mitochondrial function and nutrient sensing pathways in ageing livers. Therefore, we analyzed the effects of the aging process on mitochondrial gene expression in liver using wildtype C57BL/6N mice. In our analyses, we observed alteration in mitochondrial energy metabolism with age. To assess if defects in mitochondrial gene expression are linked to this decline, we applied a Nanopore sequencing based approach for mitochondrial transcriptomics. Our analyses show that a decrease of the Cox1 transcript correlates with reduced respiratory complex IV activity in older mice livers.

Funder

Deutsche Forschungsgemeinschaft

DFG

University Medical Center Göttingen: Universitatsmedizin Gottingen

Publisher

The Company of Biologists

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology

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