Purchase this article with an account.
S. Hoffmann, H. S. Walter, B. Seitz, M. Montenarh; Regulation of the Casein Kinase -2 in Retinal Pigment Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):488.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Proliferative vitreoretinopathy (PVR) is a common complication of failed retinal reattachment surgery. The disease is considered as a form of an exaggerated wound healing stimulated by growth factors. Retinal pigment epithelial cells (RPEs) are regarded as the main cell type responsible for vitreoretinal scars in PVR. Their proliferation, migration and contractions leads to retinal detachment and blindness. Growth factors and cytokines are determinants of the disease process. Caseinkinase-2 (CK-2) is a cell signalling molecule involved in epithelial- mesenchymal transition. Until now, the regulation, function and expression of CK-2 in RPE cells has not been enlightened. Therefore the regulation of CK-2 by the PVR associated growth factors PDGF and bFGF was investigated.
Bovine RPE cells were stimulated with the growth factors bFGF (10 ng/ml) and PDGF (10 ng/ml) for 24 hours and 48 hours in DMEM with 1% fetal growth serum (FBS). Unstimulated bovine RPE cells in DMEM with 1% FBS were used as a control. After this time course the activity of the CK-2 was evaluated with a Western Blot. Densitometry of the Western Blot Gel was done for quantification purposes. Furthermore, the modulation ofCK-2 in RPE cells by the specific inhibitors TBB and Quin was investigated. In addition, the effect of simultaneous bFGF and PDGF-BB stimulation and CK-2 inhibition on RPE cell proliferation was investigated by an MTT-assay.
The PVR associated growth factors bFGF and PDGF-BB have no impact on the expression of CK-2 in RPE cells. Furthermore, these growth factors can not abolish the inhibitory effects of CK-2 blockage on RPE cell proliferation.
CK-2 expression in RPE cells is not modulated by the PVR associated growth factors bFGF and PDGF-BB. CK-2 seems to have impact on the inhibition of RPE cell proliferation most likely by modulating cellular apoptosis.
This PDF is available to Subscribers Only