Retraction: Endothelial cell-specific deficiency of the adenosine deaminase ADAR1 aggravates LPS-induced lung injury in mice via an MDA5-independent pathway

FEBS Letters

article

Xiao-Lin Wang¹  Ru Yan³  Zhen Zhang¹  Guang-Zhi Cong²  Zhong-Jie Yi⁴  Yi-Ping Leng¹  Alex F. Chen¹ 

[1] Center for Vascular Disease and Translational Medicine, The Third Xiangya Hospital of Central South University;Department of Cardiology, The Third Xiangya Hospital of Central South University;Heart Centre, General Hospital of Ningxia Medical University;Department of Hepatobiliary Surgery, The Third Xiangya Hospital of Central South University;Institute for Cardiovascular Development and Regeneration, Xinhua Hospital Affiliated to Shanghai Jiaotong University School ofMedicine

关键词: ADAR1;    apoptosis;    endothelial cell;    lipopolysaccharide;    lung injury;    MDA5;   

DOI  :  10.1002/1873-3468.13754

来源: John Wiley & Sons Ltd.

【 摘 要 】

Adenosine deaminase acting on RNA 1 (ADAR1) has been shown to participate in the regulation of endothelial cells (ECs), as well as local and systemic inflammatory responses. Here, we find that bacterial lipopolysaccharide (LPS)-induced upregulation of ADAR1 in lung ECs is impaired in aged mice, an animal model with high rates of sepsis and mortality. Endothelial cellspecific ADAR1 knockout (ADAR1ECKO) mice suffer from higher mortality rates, aggravated lung injury, and increased vascular permeability under LPS challenge. In primary ADAR1 knockout ECs, expression of the melanoma differentiation-associated gene 5 (MDA5), a downstream effector of ADAR1, is significantly elevated. MDA5 knockout completely rescues the postnatal offspring death of ADAR1ECKO mice. However, there is no reduction in mortality or apoptosis in lung cells of ADAR1ECKO/MDA5-/- mice challenged with LPS, indicating the involvement of an MDA5-independent mechanism in this process.

【 授权许可】

Unknown