Abstract
BackgroundTrabecular meshwork (TM) plays an important role in maintaining normal intraocular pressure (IOP). Studies have shown that glaucomatous TM tissues are stiffer than those of normal tissue. The high expression of fibronectin protein (FN) and adaptor protein (LNK) may be related to high resistance to aqueous humor outflow as well as high IOP. Our concern is what factors lead to the variation of the stiffness of trabecular tissue/cells.MethodsAtomic force microscope (AFM) and Western blot (WB) analysis were applied to test TM cells of rats cultured with different concentrations of dexamethasone (DEX) and mifepristone (MIF). Rat TM cells were randomly divided into 7 groups, marked as D1, D2, D3 and M1, M2 M3 for different concentrations of DEX and MIF, respectively, and C for blank control.ResultsThe elastic modulus of the treated cells were 2.67 ± 0.914 KPa, 2.92 ± 0.986 KPa, 4.52 ± 1.22 KPa for D1, D2, D3, 2.06 ± 0.745 KPa, 1.23 ± 0.462 KPa, 0.467 ± 0.275 KPa for M1, M2, M3, and 2.43 ± 0.713 KPa for C group, respectively. Expressions of FN and LNK increase (decrease) with the increase of the concentrations of DEX (MIF).DiscussionWe focus on the relationship between the stiffness and the expressions of FN and LNK of rat TM cells. We analyzed the correlation between cell stiffness and FN, LNK expression, discussed the relationship between cell stiffness and aqueous humor outflow resistance.ConclusionsThe changes of TM cell stiffness and the expressions of FN and LNK are positively correlated.
Highlights
Trabecular meshwork (TM) plays an important role in maintaining normal intraocular pressure (IOP)
On one hand, the increased production of extracellular matrix (ECM) components in the chamber angle by TM cells may be in part responsible for the development of increased IOP [7,8,9], the increased fibronectin protein (FN) synthesis could result in a concomitant increase in IOP [10], and there is an abundance of collagen in TM samples of trabeculectomy specimens from glaucomatous eyes compared to those in the control samples [11]
Compared with the D3 group, TM cell stiffness can change about tenfold compared to the M3 group, and with the increase of DEX (MIF) concentration, TM stiffness increased
Summary
Trabecular meshwork (TM) plays an important role in maintaining normal intraocular pressure (IOP). One of the important risk factors for glaucoma is high intraocular pressure (IOP) [1, 2] that is mainly caused by increased resistance to aqueous humor outflow within the conventional outflow pathway [3,4,5]. On one hand, the increased production of extracellular matrix (ECM) components in the chamber angle by TM cells may be in part responsible for the development of increased IOP [7,8,9], the increased FN synthesis could result in a concomitant increase in IOP [10], and there is an abundance of collagen in TM samples of trabeculectomy specimens from glaucomatous eyes compared to those in the control samples [11] These findings suggest that increased ECM deposition in the outflow pathway may cause resistance to aqueous outflow and high IOP.
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