M1 microglia disrupt the barrier function of retinal microvascular endothelial cells via ANGPT2/TIE2 axis

Within retinal neurovascular unit, glial cells and microvascular endothelial cells the barrier's function and permeability. However, the cellular communications among these cells are not fully illustrated. In current study, human microglial clone 3 cells (HMC3) was induced to M1 or M2 status, then co-cultured with retinal microvascular endothelial cells (hRMECs) in vitro . We observed that M1 microglia cells could reduce the expression of tight junction of hRMECs. Furthermore, ANGPT2/ TIE2 as a novel cellular communication manner was found to be elevated in M1 HMC3 and hRMECs in co-culture system. PI3K/Akt and MAPK/ERK were involved in responding to ANGPT2/TIE2 in hRMECs for damaged barrier function. Taken together, our discovery indicates the ANGPT2/TIE2 axis as a novel cellular communication between microglia cells and retinal microvascular endothelial cells in vitro to modulate the function of the blood–retinal barrier.