Endothelin receptor-specific control of endoplasmic reticulum stress and apoptosis in the kidney.

ABSTRACT: Endothelin-1 (ET-1) promotes renal damage during cardiovascular disease; yet, the molecular mechanisms involved remain unknown. Endoplasmic reticulum (ER) stress, triggered by unfolded protein accumulation in the ER, contributes to apoptosis and organ injury. These studies aimed to determine whether the ET-1 system promotes renal ER stress development in response to tunicamycin. ET_B deficient (ET_B def) or transgenic control (TG-con) rats were used in the presence or absence of ET_A receptor antagonism. Tunicamycin treatment similarly increased cortical ER stress markers in both rat genotypes; however, only ET_B def rats showed a 14-24 fold increase from baseline for medullary GRP78, sXBP-1, and CHOP. Pre-treatment of TG-con rats with the ET_A</

SUBMITTER: De Miguel C 

PROVIDER: S-EPMC5322462 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature