Spatio-temporal expression of paired immunoglobulin-like receptor-B in the adult mouse brain after focal cerebral ischaemia. (8th August 2013)

• Record Type: Journal Article
• Authors: Gou, Xingchun; Zhang, Qiaomei; Xu, Ning; Deng, Bin; Wang, Huiwen; Xu, Lixian; Wang, Qiang
• Is Part Of: Brain injury. Volume 27:Number 11(2013)
• Page Start: 1311
• Page End: 1315
• Publication Date: 2013-08-08
• Subjects: Axonal regeneration -- ischaemia -- paired immunoglobulin-like receptor-B -- stroke; Brain damage -- Periodicals; Brain -- Wounds and injuries -- Periodicals; Brain Injuries -- Periodicals; 617.481
• DOI: 10.3109/02699052.2013.812241
• Languages: English
• ISSNs: 0269-9052

Abstract

Abstract: Primary objective : Paired immunoglobulin-like receptor-B (PirB) is another receptor, except for the Nogo receptor, that is involved in inhibition of axons regeneration after central nervous system injury. However, the expression of PirB in focal cerebral ischaemic brain remains unclear. Herein, this study investigated spatial-temporal expression of PirB in the mouse brain following transient focal cerebral ischaemia. Methods and procedure : Adult male C57BL/6 mice underwent a 60-minute transient occlusion of middle cerebral artery. Mice were killed and brain samples were harvested at 30 minutes, 2 hours, 24 hours, 3 days and 7 days after reperfusion. Expression of PirB in the brain was determined by reverse transcriptase-polymerase chain reaction (RT-PCR), western blot analysis and immunohistochemical staining. Main outcomes and results : The results showed that PirB was mainly expressed in ischaemic penumbra. PirB mRNA and protein expression began to increase at 2 hours, peaked at 24 hours and lasted for 7 days after reperfusion in the ischaemic penumbra. By using immunofluorescence, PirB signals were co-localized with NeuN-positive neurons. Conclusion : PirB expression is up-regulated in ischaemic penumbra following transient focal cerebral ischaemia. PirB expression in neurons may play important pathological roles in the inhibition of axonal regeneration after stroke, suggesting that the inhibition of PirB expression may enhance axonal regeneration and functional recovery after stroke.