DOK3降解是小鼠LPS诱导的急性呼吸窘迫综合征的发展所需

Title:DOK3 Degradation is Required for the Development of LPS-induced ARDS in Mice

Volume: 16 Issue: 4

Author(s): Ning Liu, Xiaofeng Liu, Xiaoou Li, Kaifang Duan, Yuming Deng, Xiuyan Yu, Qisheng Peng

Affiliation:

关键词: DOK3，ARDS，LPS，慢病毒，降解，表达。

摘要: It has been reported that DOK3 protein negatively regulates LPS responses and endotoxin tolerance in mice. However, the role of DOK3 in the development of acute respiratory distress syndrome (ARDS) remains unknown. In this study, we showed that DOK3 is degraded in the lung tissues of LPS-induced ARDS. Through lentivirus transduction containing DOK3(K27R) via the intranasal route, we created a mice model, in which DOK3 maintains stable expression. We found that the forced DOK3 expression significantly attenuated LPS-induced pulmonary histological alterations, inflammatory cells infiltration, lung edema, as well as the generation of inflammatory cytokines TNFα, IL- 1β and IL-6 in BALF of LPS-induced ARDS mice. In addition, DOK3 expression apparently suppressed LPS-induced NF-κB and ERK activation. These data suggested that DOK3 expression negatively regulates the development of LPS-induced ARDS in mice.

Cite this article as:

Ning Liu, Xiaofeng Liu, Xiaoou Li, Kaifang Duan, Yuming Deng, Xiuyan Yu, Qisheng Peng , DOK3 Degradation is Required for the Development of LPS-induced ARDS in Mice, Current Gene Therapy 2016; 16 (4) . https://dx.doi.org/10.2174/1566523216666161103142342