IL-6 cytoprotection in hyperoxic acute lung injury occurs via suppressor of cytokine signaling-1-induced apoptosis signal-regulating kinase-1 degradation.

ABSTRACT: Hyperoxic acute lung injury (HALI) is characterized by a cell death response that is inhibited by IL-6. Suppressor of cytokine signaling-1 (SOCS-1) is an antiapoptotic negative regulator of the IL-6-mediated Janus kinase-signal transducer and activator of transcription signaling pathway. We hypothesized that SOCS-1 is a critical regulator and key mediator of IL-6-induced cytoprotection in HALI. To test this hypothesis, we characterized the expression of SOCS-1 and downstream apoptosis signal-regulating kinase (ASK)-1-Jun N-terminal kinase signaling molecules in small airway epithelial cells in the presence of H(2)O(2), which induces oxidative stress. We also examined these molecules in wild-type and lung-specific IL-6 transgenic (Tg(+)) mice exposed to 100% oxygen for 72 hours. In control

SUBMITTER: Kolliputi N 

PROVIDER: S-EPMC2645529 | biostudies-literature | 2009 Mar

REPOSITORIES: biostudies-literature