Dexamethasone inhibits TGF-β2-induced migration of human lens epithelial cells: implications for posterior capsule opacification prevention.

The elevation of transforming growth factor-beta(2) (TGF-beta(2)) levels in eye tissue is considered as one of the major factors contributing to posterior capsule opacification (PCO) in patients undergoing cataract surgery, since TGF-beta(2) is known to stimulate the cell migration of residual human lens epithelial cells (HLECs). The present study aimed to test the potential effect of dexamethasone (DEX) on TGF-beta(2)-induced cell migration and the possible cellular mechanisms involved in this process. Cultured HLE-B3 cells were treated with TGF-beta(2) (0.1 ng/ml) in the presence or absence of DEX (100 nM). HLE-B3 cell migration was determined by the Phagokinetic Track Motility Assay. Activation of mitogen-activated protein kinase (MAPK) signaling pathways was determined by Western blotting using specific phosphorylation antibodies, matrix metalloproteinase (MMP)-2 and MMP-9 mRNA expression, and activities were analyzed by RT-PCR and gelatin zymography assay, respectively. In cultured HLE-B3 cells, DEX largely inhibited TGF-beta(2)-induced cell migration and MMP activity, probably by inhibiting the ERK/MAPK pathway. We suggest that the use of DEX may be of help in the prevention of PCO formation and development.