Tunicamycin induced ER stress in liver of C57Bl/6N mice
Description
Once protein synthesis is excessive or misfolded protein become aggregated that eventually overwhelm the capacity of the endoplasmic reticulum (ER), a state named ER stress would be reached. ER stress could affect many tissues, especially liver, in which non-alcoholic fatty liver disease, liver steatosis, etc. have been reported relative. But there still lack systematic insight into ER stress in liver, which can be obtained by integrating metabolomics and transcriptomics of the tissue. Here, tunicamycin was utilized to induce ER stress in C57BL/6N mice. Microarray and untargeted metabolomics were performed to identify the genes and metabolites significantly altered. Surprisingly, apart from classical unfolded protein response, liver lipid, arginine and proline metabolism were affirmed to be related with ER stress. And ketone body metabolism changed most prominently in ER stress, with few studies backing. What’s more, succinate receptor 1(Sucnr1) may be a novel marker and therapeutical target of liver ER stress. In this study, combination of metabolome and transcriptome provided reliable information about liver pathological processes, markers and even potential targets involved in liver ER stress.