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.
Keyphrases
- transcription factor
- poor prognosis
- cerebral ischemia
- resting state
- white matter
- endothelial cells
- binding protein
- extracellular matrix
- subarachnoid hemorrhage
- nitric oxide
- functional connectivity
- gene expression
- dna methylation
- plasmodium falciparum
- blood brain barrier
- high fat diet induced
- brain injury
- genome wide
- long non coding rna
- multiple sclerosis
- signaling pathway
- early onset
- copy number
- vascular endothelial growth factor
- cell cycle arrest
- circulating tumor cells
- endoplasmic reticulum stress
- smoking cessation