Objective To investigate the expression of PTEN and P-PTEN(the form of phosphorylated PTEN) in retinal, accordingly, to make anapproach to the functions of PTEN and P-PTEN in retinal ganglion cells(RGCs) apoptosis and survival and their functions in axonal regenerationafter partial optic nerve injury.Method 54 adult male Wistar rats were randomly selected for operation and divided into 9 groups, 6 per group. 8 of these 9 groups were operated a transient right retina clipping injury in fossa orbitalis by using retina-nip and left retina acted as normal control, 6 rats of another group were operated a sham operation(just exposed the optic nerve but no clipping injury, sacrificed after a week.). The operated rats were sacrificed either 6 hours(h) or 1, 3, 5, 7, 9, 14, 28 days(d) post operation. Immunocytochemistry were used to examine the changes of PTEN and P-PTEN in GCL and INL. All images of slices were gathered and the data were processed by using the image analyzing computer workstation of Motic image advanced 3.2 ,and then ,we analyzed the data of average gray scale by using SPSS 12.0 .Result There were expressions of PTEN and P-PTEN in normal retinal GCL and INL. By compared with normal control, the level of PTEN expressions increased markedly both in GCL of 1d,3d,5d,7d, 9d group and in INL of 7d and 9d group(P<0.01) following optic nerve injury. P-PTEN expressed highly and markedly in GCL of 6h,1d,7d,9d,14d group and in INL of 6h,1d,7d,9d group(P<0.01). In 28d group,the expression of P-PTEN decreased markedly both in GCL and INL. There was no difference of the average gray scale between the sham operation group and normal control.Conclusion There were expressions of PTEN and P-PTEN in normal retinal GCL and INL . In different time points after optic nerve injury, there were markedly changing expressions of PTEN and P-PTEN in GCL and INL, all these results suggest that the spatiotemporal profile of total PTEN and p-PTEN expressions maybe acts a important role in the progress of RGCs' apoptosis and survival and in regulating the axonal regeneration after optic nerve injury. |