Protein kinase CK2 in TGFβ-induced lens epithelial-mesenchymal transition

Cataract is a leading cause of reversible blindness. Secondary cataract is the result of migration, proliferation, and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs), induced by transforming growth factor beta (TGF beta). The extracellular signal-regulated kinases 1 and 2 (ERK 1/2) and casein kinase 2 (CK2) are important for fundamental cellular processes. This study aimed to evaluate the role of CK2 in the EMT of LECs. Primary LECs cultures were obtained from age-related and type 2 diabetes-induced cataracts. Diabetic LECs were capable of spontaneous in vitro differentiation. Treatment of LECs with TGF beta 2-stimulated ERK1/2 activity, which correlated with the expressed alpha-smooth muscle actin (alpha-SMA). siRNA-mediated attenuation of the endogenous catalytic subunit (alpha) of CK2-inhibited ERK1/2 activity and decreased alpha-SMA expression. This study shows evidence that the function of ERK1/2 is regulated by the constitutively active heterotetrameric protein kinase CK2 in this cellular phenotype. This study enriches the knowledge on LECs physiology in normal and in pathological conditions.

Automated summary

This study indicates that in diabetic-induced cataracts, CK2 affects the EMT process of LECs by regulating ERK1/2 activity. These findings enrich the understanding of LECs physiology in both normal and pathological conditions.