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Erg mediates downregulation of claudin‐5 in the brain endothelium of a murine experimental model of cerebral malaria
Author(s) -
Liu Fuhong,
Liu Qiang,
Yuan Fangshu,
Guo Shuling,
Liu Jinzhi,
Sun Zongguo,
Gao Peng,
Wang Yu,
Yan Suhua,
Liu Ju
Publication year - 2019
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13526
Subject(s) - claudin , cerebral malaria , downregulation and upregulation , gene silencing , tight junction , blood–brain barrier , microbiology and biotechnology , endothelium , transcription factor , chemistry , gene expression , vascular permeability , in vitro , biology , immunology , gene , endocrinology , central nervous system , malaria , biochemistry , plasmodium falciparum
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 ( bE nd3) 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 bE nd3 cells exposed to ECM plasma, decreased expression of claudin‐5 and Erg, and increased permeability were observed. Silencing of Erg significantly reduced Cldn5 expression. Ch IP 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.