Characterising the Role of HSPGs in Aqueous and FGF-2 - Induced Lens Epithelial Cell Proliferation

Abstract

Multiple studies have clearly identified the growth factors that promote lens epithelial cell differentiation, however there is a paucity of literature outlining the growth factors responsible for lens cell proliferation. Studies have ascertained a number of growth factors to induce the mitogen-activated protein kinase extracellular regulated signal pathway MAPK/ERK1/2, including a combination of growth factors in the aqueous humour that initiate proliferation. The growth factor FGF-2 is relevant in the role of activating a surge of signalling pathways, and the ERK1/2 profile has been shown to be essential for proliferation. It is yet to be determined how the duration of ERK1/2 signalling leads to a defined cellular response, and how the duration of ERK1/2 may correspond to differences in the receptor phosphorylation state by other kinases and phosphatases, as well as regulation of the receptor tyrosine kinase and its associated heparan sulfate proteoglycan (HSPG). Currently, the role of HSPGs in aqueous and FGF-2 –induced ERK1/2 signaling is yet to be explored in relation to lens epithelial cell proliferation. This study provides an insight into the ways in which the disruption of HSPG sulphation by sodium chlorate inhibits FGF-2 and aqueous-induced ERK1/2 signalling and lens cell proliferation.