Open AccessSOCS-1 rescues IL-1β-mediated suppression of epithelial sodium channel in mouse lung epithelial cells via ASK-1
Author(s) -
Lakshmi Galam,
Ramani Soundararajan,
Mason Breitzig,
Ashna Rajan,
Rajashekar Reddy Yeruva,
Alexander Czachor,
Francine Harris,
Richard F. Lockey,
Narasaiah Kolliputi
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.8543
Subject(s) - epithelial sodium channel , medicine , cytokine , lung , immunology , transfection , inflammation , a549 cell , apoptosis , hyperoxia , cancer research , biology , chemistry , cell culture , sodium , biochemistry , organic chemistry , genetics
Acute lung injury (ALI) is characterized by alveolar damage, increased levels of pro-inflammatory cytokines and impaired alveolar fluid clearance. Recently, we showed that the deletion of Apoptosis signal-regulating kinase 1 (ASK1) protects against hyperoxia-induced acute lung injury (HALI) by suppressing IL-1β and TNF-α. Previously, our data revealed that the suppressor of cytokine signaling-1 (SOCS-1) overexpression restores alveolar fluid clearance in HALI by inhibiting ASK-1 and suppressing IL-1β levels. Furthermore, IL-1β is known to inhibit the expression of epithelial sodium channel α-subunit (ENaC) via a p38 MAPK signaling pathway.