| First Author | Sun JC | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 522 |
| Issue | 2 | Pages | 485-491 |
| PubMed ID | 31780259 | Mgi Jnum | J:294161 |
| Mgi Id | MGI:6453589 | Doi | 10.1016/j.bbrc.2019.11.093 |
| Citation | Sun JC, et al. (2020) Depletion of beta-arrestin 2 protects against CCl4-induced liver injury in mice. Biochem Biophys Res Commun 522(2):485-491 |
| abstractText | Acute liver injury can be caused by oxidative stress within a short period and is a common pathway to many liver diseases. The liver is vulnerable to reactive oxygen species (ROS) and free radical-mediated disorders. beta-arrestin2 was initially discovered to be a negative regulator of G protein-coupled receptor signaling. Recently, beta-arrestin2 has been found to act as a multifunctional adaptor protein and play new roles in regulating intracellular signaling networks. However, the role of beta-arrestin2 in the pathogenesis of acute liver injury is unclear. In this study, we hypothesize that beta-arrestin2 regulates acute liver injury via modulation of oxidative stress. beta-arrestin2 knockout mice were used to investigate the impacts of beta-arrestin2 on carbon tetrachloride (CCl4)-induced acute liver injury and oxidative stress. Results here suggested that beta-arrestin2 deficiency decreased serum activities of aminotransferase and alleviated liver injury induced by CCl4 injection as compared with wildtype mice. beta-arrestin2 knockout mice exhibited stronger tolerance in oxidative stress compared with wild-type mice, which was demonstrated by decreased ROS level and increased superoxide dismutase (SOD) and glutathione (GSH) in the liver. Furthermore, beta-arrestin2 deficiency significantly inhibited NOX4 (a major source of ROS) expression and the activation of the extracellular regulated kinase (ERK) and, c-Jun NH2-terminal kinase (JNK) pathways. These results suggest that beta-arrestin2 deficiency protects against CCl4-induced acute liver injury through attenuating oxidative damage and decreased ERK and JNK phosphorylation. |
