Erg mediates downregulation of claudin-5 in the brain endothelium of a murine experimental model of cerebral malaria

FEBS Letters

article

Fuhong Liu¹  Qiang Liu¹  Fangshu Yuan²  Shuling Guo²  Jinzhi Liu³  Zongguo Sun¹  Peng Gao¹  Yu Wang²  Suhua Yan⁴  Ju Liu¹ 

[1] Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University;Department of Human Parasitology, School of Medicine, Shandong University;Department of Neurology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University;Department of Cardiology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University

关键词: cerebral malaria;    claudin-5;    Erg;    permeability;    transcriptional regulation;   

DOI  :  10.1002/1873-3468.13526

来源: John Wiley & Sons Ltd.

【 摘 要 】

Cerebral malaria (CM) is a severe complication with brain vascular hyperpermeability. Claudin-5 is the major component of tight junctions. To investigate the expression of claudin-5 in CM, we established a murine experimental cerebral malaria (ECM) model and an in vitro model by treating murine brain endothelial cells (bEnd3) with plasma from ECM mice. Expression of claudin-5 and the ETS transcription factor Erg was reduced in the brain endothelium of ECM mice. In bEnd3 cells exposed to ECM plasma, decreased expression of claudin-5 and Erg, and increased permeability were observed. Silencing of Erg significantly reduced Cldn5 expression. ChIP assays indicated that Erg binds to the -813 ETS motif of the murine Cldn5 gene promoter, and the binding is decreased by treatment with ECM plasma.

【 授权许可】

Unknown