![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
Preview |
PDF (Accepted Manuscript)
- Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
3MB |
![[thumbnail of Supplementary Information]](https://edoc.mdc-berlin.de/style/images/fileicons/application_msword.png) |
MS Word (Supplementary Information)
19kB |
| Item Type: | Article |
|---|---|
| Title: | Role of kinin B(2) receptor signaling in astrocyte-driven neuroinflammation |
| Creators Name: | Tavares, Mariana R., Estrela, Gabriel R., Lavezo, Luana, Silva, Juliene L.S., Araujo, Ronaldo C., Bader, Michael and Wasinski, Frederick |
| 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. |
| Keywords: | Neuroinflammation, Bradykinin, Kinin B(2) Receptor, Lipopolysaccharides, Astrocytes, Animals, Mice |
| Source: | Cellular and Molecular Neurobiology |
| ISSN: | 0272-4340 |
| Publisher: | Springer |
| Date: | 29 January 2026 |
| Official Publication: | https://doi.org/10.1007/s10571-026-01679-w |
| PubMed: | View item in PubMed |
Repository Staff Only: item control page
