Overexpression of endothelial S1pr2 promotes blood-brain barrier disruption via JNK/c-Jun/MMP-9 pathway after traumatic brain injury in both <i>in vivo</i> and <i>in vitro</i> models.

ABSTRACT:

Objectives

The disruption of blood-brain barrier (BBB) is associated with poor outcomes of TBI patients. Sphingosine-1-phosphate receptor 2 (S1pr2), a member of the G protein-coupled receptor family, is involved in endothelial activation and the regulation of vascular integrity. We hypothesized that the inhibition of S1pr2 may alleviate BBB disruption and explored potential underlying molecular mechanisms.

Methods

Lesion volumes were assessed utilizing Nissl staining; neurological outcomes were evaluated through a battery of neurobehavioral assessments; phenotype-associated proteins were scrutinized via Western blot analysis; levels of reactive oxygen species (ROS), neuronal apoptosis, and S1pr2 expression were determined using immunofluorescence staining. The impact of S1pr

SUBMITTER: Cheng H 

PROVIDER: S-EPMC11637860 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature