Please use this identifier to cite or link to this item:
Title: Expression of angiotensin II and its receptors in the normal and hypoxic amoeboid microglial cells and murine BV-2 cells
Authors: Li, J.J.
Wu, C.Y.
Kaur, C. 
Sivakumar, V. 
Ling, E.A. 
Lu, J.
Keywords: angiotensin II
BV-2 cells
microglial cells
Issue Date: 2009
Citation: Li, J.J., Wu, C.Y., Kaur, C., Sivakumar, V., Ling, E.A., Lu, J. (2009). Expression of angiotensin II and its receptors in the normal and hypoxic amoeboid microglial cells and murine BV-2 cells. Neuroscience 158 (4) : 1488-1499. ScholarBank@NUS Repository.
Abstract: Involvement of the local angiotensin receptor system in the central nervous system is well documented, yet its cellular localization and role in the glial cells have remained elusive. This study reports expression of angiotensin II and its receptors namely, angiotensin II receptor type 1 (AT1) and angiotensin II receptor type 2 (AT2) in the amoeboid microglial cells in the neonatal rat brain. In rats subjected to hypoxia, the amount of angiotensin II released in the corpus callosal tissue was reduced as revealed by enzyme immunoassay. Expression of AT1 mRNA and protein was down-regulated after hypoxic exposure, but AT2 was up-regulated. In BV-2 cells exposed to hypoxia for 4 h, expression of AT1 mRNA was reduced but AT2 was increased. These changes were further intensified respectively in LPS-stimulated microglia. Edaravone enhanced AT1 expression but suppressed AT2 expression significantly in lipopolysaccharide-stimulated cells. Neutralization of AT2 with its antiserum significantly increased mRNA expression of tumor necrosis factor-α and interleukin-1β but decreased that of transforming growth factor-beta1. In conclusion, the present results suggest that AT1 may be linked to regulation of vasodilation for increase of blood flow in hypoxic conditions, while up-regulated expression of AT2 may reduce inflammatory responses through suppression of proinflammatory cytokines and elimination of free radicals. © 2009 IBRO.
Source Title: Neuroscience
ISSN: 03064522
DOI: 10.1016/j.neuroscience.2008.11.046
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Jan 13, 2021


checked on Jan 6, 2021

Page view(s)

checked on Jan 12, 2021

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.