UCP3 overexpression neutralizes oxidative stress rather than nitrosative stress in mouse myotubes

Abstract

a b s t r a c tThe deleterious effects of oxidants on proteins may be modified by overexpression of uncoupling protein 3 (UCP3) in skeletal muscle cells exposed to hyperoxia or H 2 O 2 . UCP3 overexpression significantly attenuated the increase in protein carbonylation in response to hyperoxia and H 2 O 2 exposures. However, antioxidant enzyme content and activity (superoxide dismutases, peroxiredoxins, glutathione peroxidase-I, and catalase) were reduced or not modified in UCP3-overexpressing myotubes exposed to oxidants. Protein nitration increased in UCP3-overexpressing cells exposed to hyperoxia, but not to H 2 O 2 . We conclude that protein oxidation rather than nitration is neutralized by UPC3 overexpression in mouse myotubes exposed to abundant reactive oxygen species.

The JAK2/STAT3 Signal Pathway Regulates the Expression of Genes Related to Skeletal Muscle Development and Energy Metabolism in Mice and Mouse Skeletal Muscle Cells

“…It has been reported that excessive expression of the UCP3 gene in human skeletal muscle can promote glucose intake and lead to enhance glucose and lipid oxidation, similarly to our results. 23,24) Our study found that the JAK2/STAT3 signal pathway might regulate the body's energy metabolism by enhancing the expression of genes that are implicated in energy metabolism.…”

Platelets Promote Mitochondrial Uncoupling and Resistance to Apoptosis in Leukemia Cells: A Novel Paradigm for the Bone Marrow Microenvironment

“…Additionally, since mitochondrial uncoupling has been reported to reduce the production of reactive oxygen species [28,29], we monitored superoxide production in OCI-AML3 cells by flow cytometry. As evidenced in Fig.…”

Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases

“…In fact, UCPs reduce the damaging effects of ROS during cardiac ischemia/reperfusion injury (Barreiro et al, 2009). UCP1 isoform is involved in thermogenesis and expressed specifically in brown adipose tissue mitochondria, in which it confers a regulated proton leak across the inner membrane, whereas the physiologic functions of the other isoforms remain unclear.…”