Histones of Neutrophil Extracellular Traps Induce CD11b Expression in Brain Pericytes Via Dectin-1 after Traumatic Brain Injury
作者机构:Department of Biochemistry and Molecular BiologySchool of Basic MedicineArmy Medical UniversityChongqing400038China Department of NeurosurgeryDaping HospitalArmy Medical UniversityChongqing400042China Molecular Biology CenterState Key Laboratory of TraumaBurnand Combined InjuryDaping HospitalArmy Medical UniversityChongqing400042China Department of PathophysiologyCollege of High Altitude MedicineArmy Medical UniversityChongqing400038China Brigade 1 of Medical UndergraduatesSchool of Basic MedicineArmy Medical UniversityBattalion 1Chongqing400038China
出 版 物:《Neuroscience Bulletin》 (神经科学通报(英文版))
年 卷 期:2022年第38卷第10期
页 面:1199-1214页
核心收录:
学科分类:1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 1001[医学-基础医学(可授医学、理学学位)] 100602[医学-中西医结合临床] 10[医学]
基 金:This work was supported by the National Natural Science Foundation of China(32000670 and 82071779) Chongqing Research Program of Basic Research and Frontier Technology(cstc2017jcyjAX0338)
主 题:Pericyte Neutrophil TBI NET Dectin-1
摘 要:The brain pericyte is a unique and indispensable part of the blood-brain barrier(BBB),and contributes to several pathological processes in traumatic brain injury(TBI).However,the cellular and molecular mechanisms by which pericytes are regulated in the damaged brain are largely ***,we show that the formation of neutrophil extracellular traps(NETs)induces the appearance of CD11b^(+)pericytes after *** CD11b^(+)pericyte subsets are characterized by increased permeability and pro-inflammatory profiles compared to ***,histones from NETs by Dectin-1 facilitate CD11b induction in brain pericytes in PKC-c-Jun dependent manner,resulting in neuroinflammation and BBB dysfunction after *** data indicate that neutrophil-NET-pericyte and histone-Dectin-1-CD11b are possible mechanisms for the activation and dysfunction of *** NETs formation and Dectin-1 are promising means of treating TBI.