When rhegmatogenous retinal detachment occurs, tumor necrosis factor-alpha 
(TNF-α) among other cytokines leaks into the subretinal space, induces resident 
retinal pigment epithelial (RPE) cells to migrate, which is the initial step of 
proliferative vitreoretinopathy (PVR). In the current study, we aim to 
understand how this is regulated by focusing the cellular mechanisms involved. 
Here we identified an Akt/Tuberous sclerosis protein 2 (TSC2)/mTOR complex1 
(mTORC1) signaling pathway after TNF-α treatment to mediate RPE cell migration. 
Suppression of mTORC1 activation, either by its inhibitor rapamycin, or by 
activation of its suppressor AMP activated protein kinase (AMPK), inhibited 
TNF-α-mediated RPE cell migration, while RNA interference (RNAi)-mediated 
knocking-down of SIN1 or Rictor, two key components of mTOR complex 2 (mTORC2), 
had no significant effect on TNF-α-induced RPE cell migration. Our data provide 
initial evidence that TNF-α-mediated in vitro RPE cell migration mainly requires 
Akt/mTORC1, but not mTORC2 signaling. The results of this study may lead to 
indentify novel signaling targets against PVR.