bims-resufa 2019-05-19 papers

Issue of 2019–05–19
two papers selected by
Vera Strogolova, Marquette University

Oxid Med Cell Longev. 2019 ;2019 6051262

Higd1a Protects Cells from Lipotoxicity under High-Fat Exposure.

Tong Li, Wen-Jing Xian, Yang Gao, Shuai Jiang, Qi-Hong Yu, Qi-Chang Zheng, Yong Zhang.

Hypoxia-inducible gene domain family member 1A (Higd1a) has recently been reported to protect cells from hypoxia by helping to maintain normal mitochondrial function. The potential induction of Higd1a under high-fat exposure and whether it could protect cells from oxidative stress attracted our attention. Initially, 0.4 mM oleic acid and 0.2 mM palmitate were added to the growth media of HepG2 and LO2 cells for 72 hours. We discovered increased Higd1a expression, and knocking down Higd1a impaired mitochondrial transmembrane potential and induced cell apoptosis. We then identified that elevated reactive oxygen species (ROS) is responsible for increased Higd1a expression. Furthermore, we found that ROS promoted Higd1a expression by upregulating HIF-1a and PGC-1a expressions, and these two proteins could exert synergistic effects in inducing Higd1a expression. Taken together, these data suggest that Higd1a plays positive roles in protecting cells from oxidative stress, and ROS could induce Higd1a expression by upregulating PGC-1a and HIF-1a expressions.

DOI: https://doi.org/10.1155/2019/6051262

J Exp Biol. 2019 May 16. pii: jeb.200410. [Epub ahead of print]

Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold-acclimation and anoxia.

Amanda Bundgaard, Klaus Qvortrup, Lene Juel Rasmussen, Angela Fago.

Mitochondria are important to cellular homeostasis, but can become a dangerous liability when cells recover from hypoxia. Anoxia-tolerant freshwater turtles show reduced mitochondrial respiratory capacity and production of reactive oxygen species (ROS) after prolonged anoxia, but the mechanisms are unclear. Here, we investigated whether this mitochondrial suppression originates from downregulation of mitochondrial content or intrinsic activity by comparing heart mitochondria from 1) warm (25°C) normoxic, 2) cold-acclimated (4°C) normoxic, and 3) cold-acclimated anoxic turtles. Transmission electron microscopy of heart ventricle revealed that these treatments did not affect mitochondrial volume density and morphology. Furthermore, neither enzyme activity, protein content nor supercomplex distribution of electron transport chain (ETC) enzymes changed significantly. Instead, our data imply that turtles inhibit mitochondrial respiration rate and ROS production by a cumulative effect of slight inhibition of ETC complexes. Together, these results show that maintaining mitochondrial integrity while inhibiting overall enzyme activities are important aspects of anoxia-tolerance.

Keywords: Electron microscopy; Mitochondria; Oxygen; Reactive oxygen species; Respirometry; Supercomplex

DOI: https://doi.org/10.1242/jeb.200410