SREBP1c silencing reduces endoplasmic reticulum stress and related apoptosis in oleic acid induced lipid accumulation

Authors : Erdi SOZEN, Tugce DEMIRELYALCINER, Doga DAMLA DEMIR, Berkay OZNACAR, Nesrin KARTAL OZER

Pages : 241-247

Doi:10.5472/marumj.1009096

View : 17 | Download : 7

Publication Date : 2021-10-27

Article Type : Research Paper

Abstract :Objective: Sterol regulatory element binding protein 1c insert ignore into journalissuearticles values(SREBP1c); is one of the major transcription factors that is involved in nonalcoholic fatty liver disease insert ignore into journalissuearticles values(NAFLD); development by increasing hepatic fatty acid and triglyceride synthesis. Our study aimed to investigate the interaction of SREBP1c with endoplasmic reticulum insert ignore into journalissuearticles values(ER); stress in oleic acid insert ignore into journalissuearticles values(OA); induced lipid accumulation. Material and Methods: Optimum lipid droplet insert ignore into journalissuearticles values(LD); formation and SREBP-1c induction were determined in alpha mouse liver 12 insert ignore into journalissuearticles values(AML12); hepatocytes following the incubation with different OA concentrations. To determine the effect of SREBP-1c, cells were transfected with siRNA specific for SREBP-1c. LD formation and SREBP-1c induction were determined via Oil Red O and immunblotting, respectively. Phospho IRE1, GRP78, CHOP, ATF6 and JNK levels were determined with immunofluorescence staining. Results: Optimum LD formation and SREBP-1c induction were achieved at 0.5 mM oleat concentration. While SREBP-1c silencing decreased LD formation in non-OA treated cells, no significant effect of silencing was determined following OA administration. On the other hand, SREBP-1c silencing in OA treated cells reduced phospho IRE1, ATF6, JNK and CHOP expressions. Conclusion: Our results suggest that the novel function of SREBP-1c can regulate ER stress response in OA induced lipid accumulation.
Keywords : Lipid accumulation, SREBP1c, ER stress, Apoptosis