The Effect Of ClC-3in Multiplication,Adhesion And Migration Of Lens Epithelial Cell

Object: The lens epithelial cells (LECs) is only the cell that havethe dividing ability in the lens. It not only has the growth, deffere-ntiation and damage-repair of the lens, and has an important role inmaintaining the transparent of lens and stabilizing internal environment.The exceptional multiplication and migration of LECs are the foundationswhich cataract and after-cataract form. Therefore, it is an importantcell in the mechanism study of cataract and after-cataract. Recently,the research of ion channels involved in cataract formation is graduallydeepening, especially chloride channels. The study found that majorityof the cells in vivo are CLC-3chloride channel(CLC-3), it plays animportant role in maintaining cell volume homeostasis, and extensivelyparticipating many kinds of functional such as cellproliferation,adhesion and death.This study explored the expression of CLC-3in patients with senilecataract,and reseach the role of CLC-3in LECs multiplication, adhesionand migration process with human LECs in vitro to clarify the role ofCLC-3in formation of cataract or after-cataract and provide the experi-mental basis for the prevention and treatment.Method: We studied the expression of CLC-3in lens epithelial cellsof senile cataract by using HE staining and immunohistochemistry. Wedetected the CLC-3on LECs proliferation and adhesion effect by MTTmethod; the effects of migration of CLC-3on LECs using scratch.Results: Immunohistochemical staining results found that LECs insenile cataract patients CLC-3expression was significantly increasedthan normal people, which showed that CLC-3associated with cataract disease. LECs multiplication experiments have shown that chlorine ionchannel inhibitor-NPPB which in a certain range of concentration and timedependently inhibited cell proliferation, with200μM for the best.LECs adhesion experiments have shown that NPPB4h, adhesion to the LECscompared with the control group was not obvious. But for NPPB8h and12h,adhesion50μM,100μM and200μM concentration of NPPB on LECs wassignificantly suppressed, compared with statistical differences (P <0.05). Scratch experimental results showed that, NPPB could transfer aconcentration dependent inhibition of LECs, with200μM for the best.Conclusion: CLC-3can affect the proliferation, adhesion and migrationof LECs, and inhibition of CLC-3can control the formation of cataractand after-cataract.