Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8721310 | Clinical Immunology | 2018 | 32 Pages |
Abstract
Smoke inhalation leads to acute lung injury (ALI), a devastating clinical problem associated with high mortality. Suppressor of cytokine signaling-1 (SOCS-1) is a negative regulator of apoptosis and pro-inflammatory cytokine signaling, two major contributors to the pathogenesis of ALI. We have found that SOCS-1 protects lung epithelial cells from smoke-induced apoptosis through two mechanisms. One is that SOCS-1 enhances degradation of ASK-1 and diminishes cleavage of pro-caspase-3 to repress smoke-triggered apoptosis in lung epithelial cells. The other is that SOCS-1 represses smoke-triggered DISC formation through altering TRADD-caspase-8 interaction rather than TNFR-1-TRADD interaction or TNFR-1-TRAF-2 interaction. In conclusion, SOCS-1 relieves smoke inhalation-induced lung injury by repressing ASK-1 and DISC-mediated epithelium apoptosis.
Keywords
ARDSTNF receptor-associated death domain proteinASK-1TRADDSOCS-1SH2TRAF2FADDDISCGFPTNFR1Acute lung injuryAlitumor necrosis factor alphasuppressor of cytokine signaling-1Small airway epithelial cellsAcute respiratory distress syndromeTNF receptor-associated factor 2TNF-αSrc Homology 2FAS-associated death domain proteingreen fluorescent proteindeath-inducing signaling complexApoptosis signal-regulating kinase-1tumor necrosis factor receptor 1
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Authors
Leifang Zhang, Chenming Xu, Yating Ma, Kairui Zhu, Xiaoming Chen, Qiwen Shi, Weike Su, Hang Zhao,