LPS-induced mitochondrial DNA synthesis and release facilitate RAD50-dependent acute lung injury
作者机构:Department of PulmonologyChildren’s HospitalZhejiang University School of MedicineNational Clinical Research Center for Child HealthNational Children's Regional Medical CenterHangzhouZhejiangChina International Institutes of Medicinethe Fourth Affiliated Hospital of Zhejiang University School of MedicineYiwuChina Department of Pharmacology and Department of Respiratory and Critical Care Medicine of the Second Affiliated HospitalZhejiang University School of MedicineKey Laboratory of Respiratory Disease of Zhejiang ProvinceHangzhouZhejiangChina
出 版 物:《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗(英文))
年 卷 期:2021年第6卷第4期
页 面:1104-1106页
核心收录:
学科分类:0710[理学-生物学] 1002[医学-临床医学] 10[医学]
基 金:The authors are grateful for financial support from the National Natural Science Foundation of China(81870007,81920108001,81800024,81900025,81870023,81700025) the Zhejiang Provincial Natural Science Foundation(LD19H160001) the Zhejiang Provincial Program for the Cultivation of High-Level Innovative Health Talents(2016-63).
摘 要:Dear Editor,ATP-binding cassette(ABC)-ATPase(RAD50),together with meiotic recombination 11 homolog 1(MRE11)subunits,to form MRE11-RAD50 complex,plays important roles in recognition of double-stranded DNA(dsDNA)and initiation of consequent inflammatory cascade1.Acute lung injury(ALI)and acute respiratory destress syndrome(ARDS)are systemic uncontrolled inflammation and life-threatening.However,the function of the DNA sensor in ALI/ARDS remains poorly defined.Here we investigated functions of RAD50 using mouse primary macrophages and conditionally RAD50 knockout mice in vitro and in a lipopolysaccharide(LPS)-induced lung injury model.