Abrogation of store-operated Ca²⁺ entry protects against crystal-induced ER stress in human proximal tubular cells.

ABSTRACT: Calcium crystal internalization into proximal tubular (PT) cells results in acute kidney injury, nephrocalcinosis, chronic kidney disease (CKD), and kidney-stone formation. Ca²⁺ supersaturation in PT luminal fluid induces calcium crystal formation, leading to aberrant crystal internalization into PT cells. While such crystal internalization produces reactive oxygen species (ROS), cell membrane damage, and apoptosis; the upstream signaling events involving dysregulation of intracellular Ca²⁺ homeostasis and ER stress, remain largely unknown. We have recently described a transepithelial Ca²⁺ transport pathway regulated by receptor-operated Ca²⁺ entry (ROCE) in PT cells. Therefore, we examined the pathophysiological consequence of internalization of

SUBMITTER: Gombedza FC 

PROVIDER: S-EPMC6680047 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature