NF‑κB/IκBα signaling pathways are essential for resistance to heat stress‑induced ROS production in pulmonary microvascular endothelial cells.

ABSTRACT: The results of a previous study demonstrated that heat stress (HS) triggered oxidative stress, which in turn induced the apoptosis of epithelial cells. These results uncovered a novel mechanism underlying the activation of NF‑κB in primary human umbilical vein endothelial cells. The present study aimed to further investigate the role of NF‑κB/IκBα signaling pathways in the inhibition of HS‑induced reactive oxygen species (ROS) generation and cytotoxicity in endothelial cells. The results of the present study demonstrated that HS triggered a significant amount of NF‑κB and IκBα nuclear translocation without IκBα degradation in a time‑dependent manner. Mutant constructs of IκBα phosphorylation sites (Ser32, Ser36) were employed in rat pulmonary microvascular endothelial cells (PMVECs). Cell

SUBMITTER: Xie W 

PROVIDER: S-EPMC8477608 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature