Role of Kinin B2 Receptor Signaling in Astrocyte-driven Neuroinflammation
Year: 2026
Type: article
Abstract: The kallikrein–kinin system (KKS) plays a key role in inflammatory responses, but its specific contribution to neuroinflammation remains to be fully elucidated. The bradykinin B 2 receptor (B 2 R), a principal effector of the KKS, is widely expressed in both neuronal and glial cells in the rodent and human brain. In this study, we investigated the molecular contribution of B 2 R to neuroinflammation using complementary in vitro and in vivo models. Lipopolysaccharide (LPS) stimulation significantly upregulated B 2 R mRNA expression in primary astrocyte cultures and in the cortical tissue of wild-type mice. Pharmacological blockade of B 2 R in astrocytes markedly suppressed the LPS-induced proinflammatory gene expression. In contrast, B 2 R antagonism in vivo resulted in only partial attenuation of the neuroinflammatory response. Together, these findings suggest cell type–specific roles for B 2 R and underscore its key contribution to astrocyte-mediated neuroinflammation. Graphical Abstract B 2 R antagonism highlights cell type–specific roles in neuroinflammation. B 2 R pharmacological antagonism suppresses proinflammatory gene expression in astrocytes but shows limited in vivo efficacy, indicating differential functions across brain cell types.
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $4,590
Awards: G116629194, G2705349929, G2823776494, G2887233392, G2942308653, G2945570127, G295657101, G3569778533, G4169112054, G46312875, G4687589724, G4815001938, Effects of kinin B2 receptor deletion on GABAergic neurons and neurons expressing the dopaminergic D2 receptor, G5733264535, G5960408532, G6191138830, G6719977419, G6815844370, Kinin receptor B2 participation in the nervous system with emphasis on the dopaminergic circuit, G8292535990, G864372127
OpenAlex ID: W7126052950