Differential ER stress as a driver of cell fate following ricin toxin exposure.

ABSTRACT: Inhalation of trace amounts of ricin toxin, a plant-derived ribosome-inactivating protein, results in ablation of alveolar macrophages, widespread epithelial damage, and the onset of acute respiratory distress syndrome (ARDS). While ricin's receptors are ubiquitous, certain cell types are more sensitive to ricin-induced cell death than others for reasons that remain unclear. For example, we demonstrate in side-by-side studies that macrophage-like differentiated THP-1 (dTHP-1) cells are hyper-sensitive to ricin, while lung epithelium-derived A549 cells are relatively insensitive, even though both cell types experience similar degrees of translational inhibition and p38 MAPK activation in response to ricin. Using a variety of small molecule inhibitors, we provide evidence that ER stress cont

SUBMITTER: Peterson-Reynolds C 

PROVIDER: S-EPMC8728110 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature