Open Access

ARTICLE

Loss of the ubiquitin-conjugating enzyme Rad6B disturbs mitochondrial function and cellular homeostasis in mouse skin

LINGHUI YU^#, RONG SHEN^#, YANAN GUO, YANXUAN GUO, CHEN LI, YANFENG SONG^*, DEGUI WANG^*

Department of Anatomy and Histology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China

* Corresponding Authors: Yanfeng Song. Email: ; Degui Wang. Email:

BIOCELL 2021, 45(3), 761-772. https://doi.org/10.32604/biocell.2021.014602

Received 12 October 2020; Accepted 21 December 2020; Issue published 03 March 2021

Abstract

Various factors can induce cell degeneration by altering the phenotype and metabolism of cells. Mitochondria play an essential role in cellular homeostasis and function, rendering aging processes highly associated with mitochondrial function and status. Herein, we describe an aging-prone phenotype of murine skin cells caused by depletion of Rad6B (Ube2b), an E2 ubiquitin-conjugating enzyme. In this study, using Masson’s trichrome, we showed that loss of Rad6B causes physiological structure changes in mouse skin with age. In addition, a combination of western blotting experiments, transmission electron microscopy and employment of immunofluorescence staining revealed that depletion of Rad6B was characterized by an abnormal mitochondrial metabolic profile, including decreased mitochondrial biosynthesis and mitochondrial complex activities, increased ROS production and suppressed mitophagy resulting in metabolic disorders. Taken together, these results highlight an important relationship between Rad6B and skin senescence, suggesting that Rad6B plays an indispensable role in maintaining a healthy mitochondrial network and intracellular homeostasis.

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Keywords

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