Oxidative stress-induced temporal activation of ERK1/2 phosphorylates coreceptor of Wnt/ β-catenin for myofibroblast formation in human lens epithelial cells

CONCLUSIONS: ERK1/2 signaling plays a crucial role in the moderate level of oxidative stress-induced EMT in LECs. Pharmacologically blocking ERK1/2 signaling significantly inhibited LEC proliferation and EMT. Mechanistically, ERK1/2 signaling regulated Wnt/β-catenin cascade by phosphorylating Wnt coreceptor LRP6 at Ser 1490 in the plasma membrane. These results shed light on a potential molecular switch of ERK1/2 and Wnt/β-catenin crosstalk underlying the development of PCO.PMID:38222447 | PMC:PMC10784218
Source: Molecular Vision - Category: Molecular Biology Authors: Source Type: research