heme oxygenase-2 localizes to mitochondria and regulates hypoxic responses in hepatocytes
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2018
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Abstract
Hypoxia occurs as a part of multiple disease states, including hemorrhagic shock. Adaptive responses occur within the cell to limit the consequences of hypoxia. This includes changes in mitochondrial respiration, stress-induced cell signaling, and gene expression that is regulated by hypoxia inducible factor-1α (HIF-1α). Heme oxygenase-2 (HO-2) has been shown to be involved in oxygen sensing in several cell types. The purpose of these experiments was to test the hypothesis that HO-2 is a critical regulator of mitochondrial oxygen consumption and reactive oxygen species (ROS) production to influence hypoxia-adaptive responses such as HIF-1α protein levels and JNK signaling. Methods and Results. In vitro studies were performed in primary mouse hepatocytes. HO-2, but not HO-1, was expressed in mitochondria at baseline. Decreased oxygen consumption and increased mitochondrial ROS production in response to hypoxia were dependent upon HO-2 expression. HO-2 expression regulated HIF-1α and JNK signaling in a mitochondrial ROS-dependent manner. Furthermore, knockdown of HO-2 led to increased organ damage, systemic inflammation, tissue hypoxia, and shock in a murine model of hemorrhage and resuscitation. Conclusion. HO-2 signaling plays a role in hypoxic signaling and hemorrhagic shock. This pathway may be able to be harnessed for therapeutic effects.
| Reference Key |
waltz2018oxidativeheme
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|---|---|
| Authors | ;Paul K. Waltz;Benjamin Kautza;Jason Luciano;Mitch Dyer;Donna Beer Stolz;Patricia Loughran;Matthew D. Neal;Jason L. Sperry;Matthew R. Rosengart;Brian S. Zuckerbraun |
| Journal | journal of aoac international |
| Year | 2018 |
| DOI |
10.1155/2018/2021645
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| URL | |
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