Ca2+ homeostasis and signaling disturbances are associated with lens pathophysiology and are involved in cataract formation. Here, we explored the spatiotemporal changes in Ca2+ signaling in lens epithelial cells (LECs) upon local mechanical stimulation, to better understand the LECs’ intercellular communication and its association with cataractogenesis. We were interested in if the progression of the cataract affects the Ca2+ signaling and if modifications of the Ca2+ homeostasis in LECs are associated with different cataract types. Experiments were done on the human postoperative anterior lens capsule (LC) preparations consisting of the monolayer of LECs on the basement membrane. Our findings revealed that the Ca2+ signal spreads radially from the stimulation point and that the amplitude of Ca2+ transients decreases with increasing distance. It is noteworthy that a comparison of signaling characteristics with respect to the degree of cataract progression revealed that, in LCs from more developed cataracts, the Ca2+ wave propagates faster and the amplitudes of Ca2+ signals are lower, while their durations are longer. No differences were identified when comparing LCs with regard to the cataract type. Moreover, experiments with Apyrase have revealed that the Ca2+ signals are not affected by ATP-dependent paracrine communication. Our results indicated that cataract progression is associated with modifications in Ca2+ signaling in LECs, suggesting the functional importance of altered Ca2+ signaling of LECs in cataractogenesis.

Purpose The purpose of this study is to explore and identify intra‐ and inter‐cellular calcium (Ca2+) signaling in human lens epithelial cells (LECs) upon local mechanical stimulation, to understand better the role of Ca2+ in intercellular communication related to cataract formation, lens regeneration and posterior capsular opacification (PCO). Methods The anterior lens capsule (aLC: basement membrane and associated LECs) were obtained from cataract surgery. Primary human LEC cultures were established by placing adherently the intact human aLC onto Petri dishes. LECs were stained with Fura‐2 dye, the fluorescence of which was imaged to monitor spatio‐temporal changes in cytosolic free Ca2+ concentrations in response to localized, micropipette induced mechanical stimulation. Results Analysis of the intra‐ and inter‐cellular Ca2+ signaling from postoperative aLCs and cultures showed that the Ca2+ signal spreads radially and its propagation speed increases with the degree of cataract. While in aLC Ca2+ signals travels between the first few neighbor LECs in the order of seconds, in confluent culture the propagation is slower and it covers smaller distances. LECs from aLC with less developed cataracts exhibit faster and bigger changes in intracellular Ca2+ concentration. Moreover, in aLC and in LEC cultures, the duration of Ca2+ transients prolongs with increasing distance from stimulation site, whereas their amplitude decreases. Conclusions The modifications of Ca2+ homeostasis in LECs, which are associated with different degrees of cataract, affect Ca2+ signaling upon the local mechanical stimulation. Impairment of Ca2+ signaling might be the basis of cataract formation. LEC's cultures have less developed Ca2+ signaling capabilities, what might be reflected on lens regeneration and PCO.