Published online Jul 14, 2022. doi: 10.3748/wjg.v28.i26.3201
Peer-review started: January 13, 2022
First decision: March 8, 2022
Revised: March 22, 2022
Accepted: May 13, 2022
Article in press: May 13, 2022
Published online: July 14, 2022
Processing time: 180 Days and 23.7 Hours
Endoplasmic reticulum (ER) stress plays an important role in the pathogenesis of chronic liver diseases, but how hepatocytes respond to ER stress has not been clarified. Alpha-fetoprotein (AFP) is secreted by hepatoma cells and elevated levels of serum AFP are associated with development of liver malignancies.
Anti-injury response is an important force for hepatocytes to resist liver injury mediated by various reasons, which has a close relationship to the progress and prognosis of liver injury. Studying the anti-injury mechanism of hepatocytes is important for the diagnosis and treatment of liver injury in the clinic.
To investigate whether and how AFP could regulate ER stress and hepatocyte injury.
The distribution of AFP and the degrees of ER stress in liver tissues were characterized by histology, immunohistochemistry, and Western blot in biopsied human liver specimens, two mouse models of liver injury and a cellular model. The levels of AFP in sera and the supernatants of cultured cells were quantified by chemiluminescence.
ER stress induces liver injury and increases intracellular AFP expression in hepatocytes. ER stress up-regulates intracellular AFP expression by up-regulating activating transcription factor-6 (ATF6). Upregulated AFP feedback attenuates ER stress, forming a regulatory loop. Upregulated AFP mitigates the ER stress-induced hepatocyte apoptosis and necroptosis.
ER stress upregulated intracellular AFP expression in hepatocytes by up-regulating ATF6 during the process of liver injury and intracellular AFP feedback-attenuated hepatocyte apoptosis and necroptosis by alleviating ER stress.
Intracellular AFP induced by ER stress alleviates hepatocyte apoptosis and necroptosis by activating ATF6.