SOCS-1 rescues IL-1β-mediated suppression of epithelial sodium channel in mouse lung epithelial cells via ASK-1 | Zendy

Lakshmi Galam | Zendy; Ramani Soundararajan | Zendy; Mason Breitzig | Zendy; Ashna Rajan | Zendy; Rajashekar Reddy Yeruva | Zendy; Alexander Czachor | Zendy; Francine Harris | Zendy; Richard F. Lockey | Zendy; Narasaiah Kolliputi | Zendy

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SOCS-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.

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