A Study On The Change Of The Trabecular Meshwork Cells Secreting TGF-beta2 Under The Control Of A New Culture System By Imposing A Pressure On Cells With Open Cycling Air

【Objective】By using a new culture system, which could impose pressure on cells with open cycling air, we observed the effects of the pressure on the human trabecular meshwork cells autocrining transforming growth factor-beta2 (TGF-beta2). The purpose of this study was to investigate the role of TGF-beta2 in the pathogenesis of primary open angle glaucoma.【Methods】The human trabecular meshwork cells were cultured in vitro and transferred to the 5th passage for experiments. The new culture system could control the pressure at different levels. We used it to impose pressures of 20, 40, 60 and 80 mmHg on each experiment group respectively. Furthermore, the cells had been cultured for 12, 24 and 36 hours under each pressure. Those cells cultured without any pressure imposed were taken as the control group. The concentration of TGF-beta2 was tested by enzyme-linked immunosorbent assay (ELISA). 【Results】The level of TGF-beta2 secreted by cells in experiment groups rose as the pressure increased and was significantly higher than that in control group. When the pressure below 60 mmHg, the concentration of TGF-beta2 was raising on as the time of the pressure imposed on the cells extending on. The cells cultured under 40 mmHg pressure for 36 hours autocrined TGF-beta2 with the highest level of (1305.36±105.33) pg/ml. The concentration of TGF-beta2 in the 80 mmHg pressure group was lower than that in other experiment groups, but the TGF-beta2 level in the 80 mmHg/12 hours and the 80 mmHg/24 hours groups was still significantly higher than that in the control group.【Conclusions】The rising pressure promoted the human trabecular meshwork cells to autocrine TGF-beta2 and the level was related to different pressure levels and their sustained times. These findings indicated the elevated concentration of TGF-beta2 in aqueous humor of patients might play a role in the pathogenesis of primary open angle glaucoma.