Endoplasmic-reticulum-stress-induced lipotoxicity in human kidney epithelial cells.

ABSTRACT: Accumulation of lipids and their intermediary metabolites under endoplasmic reticulum (ER) stress instigates metabolic failure, described as lipotoxicity, in the kidney. This study aimed to determine ER-stress-related sphingolipid and polyunsaturated fatty acid (PUFA) changes in human kidney cells. Tunicamycin (TM) was employed to induce ER stress and an ER stress inhibitor, tauroursodeoxycholic acid (TUDCA), was given to minimize cytotoxicity. Cell viability was determined by MTT assay. Sphingomyelin (SM), ceramide (CER), and PUFA levels were measured by LC-MS/MS. Glucose-regulated protein 78-kd (GRP78), cleaved caspase-3 and cyclooxygenase-1 (COX-1) levels were assessed by immunofluorescence. Cytosolic phospholipase A₂ (cPLA₂), total COX, and prostaglandin E_2</

SUBMITTER: Ceker T 

PROVIDER: S-EPMC9424710 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature