1Department of Neonatology, Children’s Hospital of Fudan University, Shanghai 201102, China
2Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
Corresponding author: Guo-Qiang Cheng. E-mail: gqchengcm@sina.com

Abstract 

Neonatal sepsis is common in neonatal intensive care units, often complicated by injury to the immature brain. Previous studies have shown that the expression of the gap junction protein connexin 43 (Cx43) in the brain decreases when stimulated by neuro-inflammatory drugs such as lipopolysaccharide (LPS). Here we showed that partial deletion of Cx43 in astrocytes resulted in weakened inflammatory responses. The up-regulation of pro-inflammatory cytokines was significantly reduced in mice with partial deletion of Cx43 in astrocytes compared with wild-type littermates after systemic LPS injection. Moreover, microglial activation was inhibited in mice with partial deletion of Cx43. These results showed that Cx43 in astrocytes plays a critical role in neuro-inflammatory responses. This work provides a potential therapeutic target for inhibiting neuro-inflammatory responses in neonatal sepsis.

Keywords

astrocyte; gap junction; Cx43; neonatal sepsis

[SpringerLink]