| First Author | Huang T | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 477 |
| Issue | 4 | Pages | 932-936 |
| PubMed ID | 27402274 | Mgi Jnum | J:238671 |
| Mgi Id | MGI:5823336 | Doi | 10.1016/j.bbrc.2016.07.001 |
| Citation | Huang T, et al. (2016) Increase of p25 associated with cortical neuronal death induced by hypoxia. Biochem Biophys Res Commun 477(4):932-6 |
| abstractText | The mechanisms of neuronal damage in hypoxic cerebral cortex are complicated. Recent studies indicated that deregulation of Cdk5 was involved in neuronal death induced by hypoxia (1% O2). However, the pathological effect of Cdk5 is not fully elucidated. Therefore, in order to decipher the effect of Cdk5 on cellular death in hypoxic condition, the Cdk5 and its activator p35/p25 were investigated in cortical neurons at 10 DIV (Days In Vitro). Upon exposure to hypoxia, the cortical neurons showed a time-dependent increase of neuronal death compared to normoxia-treated control neurons. In correlation to the increase of neuronal death under hypoxia, the level of p25, a truncated form of p35, also increased in a time-dependent manner. Importantly, inhibition of Cdk5 kinase activity by roscovitine protected neurons from death under hypoxic stress. In contrast, ectopic upregulation of Cdk5 kinase activity in neurons expressing p25 led to an increase of neuronal death in comparison to control neurons expressing GFP. It suggests that ectopic increase of Cdk5 kinase activity through conversion of p35 to p25 is involved in the process of neuronal death induced by hypoxia. |
