| First Author | Li M | Year | 2015 |
| Journal | J Neurochem | Volume | 134 |
| Issue | 2 | Pages | 211-21 |
| PubMed ID | 25824575 | Mgi Jnum | J:224556 |
| Mgi Id | MGI:5688250 | Doi | 10.1111/jnc.13110 |
| Citation | Li M, et al. (2015) Vinexin-beta deficiency protects against cerebral ischaemia/reperfusion injury by inhibiting neuronal apoptosis. J Neurochem 134(2):211-21 |
| abstractText | Vinexin-beta is an adaptor protein that regulates cell adhesion, cytoskeletal organization and signal transduction. Our previous work showed that Vinexin-beta protects against cardiac hypertrophy. However, its function in stroke is largely unknown. In the present study, we observed a significant increase in Vinexin-beta expression in both human intracerebral haemorrhage and mouse cerebral ischaemia/reperfusion (I/R) injury model, indicating that Vinexin-beta is involved in stroke. Next, using Vinexin-beta knockout mice, we further demonstrated that Vinexin-beta deficiency significantly protected against cerebral I/R injury, as demonstrated by a dramatic decrease in the infarct volume and an improvement in neurological function. Additionally, immunofluorescence and western blotting showed that the deletion of Vinexin-beta attenuated neuronal apoptosis. Mechanically, we found that Akt signalling was up-regulated in the brains of the Vinexin-beta knockout mice compared with those of the WT control mice after ischaemic injury. Taken together, our results demonstrate that the deletion of Vinexin-beta potently protects against ischaemic injury by inhibiting neuronal apoptosis, and this effect may occur via the up-regulation of Akt signalling. Our findings revealed that Vinexin-beta acts as a novel modulator of ischaemic injury, suggesting that Vinexin-beta may represent an attractive therapeutic target for the prevention of stroke. |
