Vinexin‐β deficiency protects against cerebral ischaemia/reperfusion injury by inhibiting neuronal apoptosis

Vinexin‐β is an adaptor protein that regulates cell adhesion, cytoskeletal organization and signal transduction. Our previous work showed that Vinexin‐β protects against cardiac hypertrophy. However, its function in stroke is largely unknown. In the present study, we observed a significant increase in Vinexin‐β expression in both human intracerebral haemorrhage and mouse cerebral ischaemia/reperfusion (I/R) injury model, indicating that Vinexin‐β is involved in stroke. Next, using Vinexin‐β knockout mice, we further demonstrated that Vinexin‐β 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‐β attenuated neuronal apoptosis. Mechanically, we found that Akt signalling was up‐regulated in the brains of the Vinexin‐β knockout mice compared with those of the WT control mice after ischaemic injury. Taken together, our results demonstrate that the deletion of Vinexin‐β 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‐β acts as a novel modulator of ischaemic injury, suggesting that Vinexin‐β may represent an attractive therapeutic target for the prevention of stroke. Vinexin‐β is an adaptor protein that regulates cell adhesion and cytoskeletal organization. We revealed that Vinexin‐β‐deficient mice are potently protected against ischaemia/reperfusion (I/R) injury. The protective effect is mediated through inhibiting neuronal apoptosis, which may occur via the up‐regulation of Akt signalling. These findings suggest Vinexin‐β as a novel regulator of I/R injury and attractive therapeutic target for the prevention of stroke. Vinexin‐β is an adaptor protein that regulates cell adhesion and cytoskeletal organization. We revealed that Vinexin‐β‐deficient mice are potently protected against ischaemia/reperfusion (I/R) injury. The protective effect is mediated through inhibiting neuronal apoptosis, which may occur via the up‐regulation of Akt signalling. These findings suggest Vinexin‐β as a novel regulator of I/R injury and attractive therapeutic target for the prevention of stroke.