Feedback loop centered on MAF1 reduces blood-brain barrier damage in sepsis-associated encephalopathy.

ABSTRACT:

Background

A previous study found that MAF1 homolog, a negative regulator of RNA polymerase III (MAF1), protects the blood-brain barrier (BBB) in sepsis-associated encephalopathy (SAE); however, the related molecular mechanisms remain unclear.

Subjects and methods

In this study, a rat sepsis model was constructed using the cecum ligation and puncture (CLP) method. In vitro, rat brain microvascular endothelial cells and astrocytes were stimulated with serum from the sepsis model rats. The loss of MAF1 protein levels and the molecular mechanisms leading to cell damage were investigated.

Results

It was shown in the SAE models that MAF1 was expressed at low levels. Knockdown of Cullin 2 (CUL2) stimulated the accumulation of MAF1 protein, attenuated the RNA sensor RIG-I/in

SUBMITTER: Wei X 

PROVIDER: S-EPMC11744841 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature