Na/K-ATPase suppresses LPS-induced pro-inflammatory signaling through Lyn.

ABSTRACT: Na/K-ATPase (NKA), besides its ion transporter function, is a signal transducer by regulating Src family kinases (SFK). The signaling NKA contributes to oxidized LDL-induced macrophage foam cell formation and interacts with TLR4. However, its role in lipopolysaccharides (LPS)-induced signaling and glycolytic switch in macrophages remains unclear. Using peritoneal macrophages from NKA α1 haploinsufficient mice (NKA α1^+/-), we found that NKA α1 haploinsufficiency led to enhanced LPS-stimulated NF-κB pathway, ROS signaling, and pro-inflammatory cytokines. Intraperitoneal injection of LPS resulted in more severe lung inflammation and injury with lower survival rate in NKA α1^+/- mice. Additionally, LPS induced a higher extent of the metabolic switch from oxidative phosphor

SUBMITTER: Zhang J 

PROVIDER: S-EPMC9442361 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature