| First Author | Jin G | Year | 2005 |
| Journal | J Cereb Blood Flow Metab | Volume | 25 |
| Issue | 3 | Pages | 302-13 |
| PubMed ID | 15647743 | Mgi Jnum | J:112482 |
| Mgi Id | MGI:3656406 | Doi | 10.1038/sj.jcbfm.9600021 |
| Citation | Jin G, et al. (2005) Deficiency of PAR-2 gene increases acute focal ischemic brain injury. J Cereb Blood Flow Metab 25(3):302-13 |
| abstractText | The expression profile of the protease-activated receptor-2 (PAR-2) and effects of PAR-2 gene knockout (PAR-2 KO) on the infarct size were investigated after 60 minutes of transient middle cerebral artery occlusion (tMCAO) in mice in relation to phosphorylated extracellular signal-regulated kinase (p-ERK) and astrocyte activation. PAR-2 was normally distributed mainly in neurons of the central nervous system (CNS), and strongly upregulated at 8-24 hours after tMCAO. Deficiency of PAR-2 gene significantly increased the infarct volume and the number of TUNEL-positive cells at 24 hours of reperfusion. The strong neuronal expression of p-ERK was induced at 5 minutes as a peak after reperfusion in wild-type mice, but the signal change was significantly reduced in PAR-2 KO mice. Astroglial activation was also greatly inhibited at 24 hours after tMCAO in PAR-2 KO mice. These results show that the deficiency of PAR-2 gene increases the acute ischemic cerebral injury associating with suppression of neuronal ERK activation and reactive astroglial activation. |
