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【文摘发布】小梁细胞过度合成细胞外基质的作
Tane N, Dhar S, Roy S, Pinheiro A, Ohira A, Roy S.
Department of Medicine, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA; Department of Ophthalmology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA; Department of Ophthalmology, Shimane University Faculty of Medicine, 89-1, Enya, Izumo, Shimane, 693-8501, Japan.
The extracellular matrix (ECM) of the trabecular meshwork (TM) is an important determinant of its functional properties. This study was performed to investigate whether overexpression of ECM components, laminin (LM) and collagen type IV (Col) by TM cells may play a role in the development of outflow resistance. To determine the effect of excess LM and Col expression on cell monolayer permeability, an in vitro cell culture model was used in which overexpression of the two ECM components, LM and Col, was induced by high glucose (HG) (30mM) or 0.1muM dexamethasone (D) in bovine and human trabecular meshwork (BTM and HTM) cells. Western blot analysis and immunofluorescence staining confirmed increased LM and Col synthesis in cells exposed to HG or D. Increased level of LM and Col protein resulted in reduced cell monolayer permeability. Transfection with antisense oligos (AS-oligos) targeted against LM or Col inhibited HG- or D-induced LM and Col gene overexpression in TM cells with concomitant increase in permeability. The AS-oligo strategy was effective in reducing LM or Col level in the TM cells in all conditions tested in this study. These findings suggest that increased LM and Col deposition in the outflow pathway may cause resistance to aqueous outflow and contribute to the development of primary open angle glaucoma (POAG).
PMID: 17350618 [PubMed - as supplied by publisher] 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 题目：Effect of excess synthesis of extracellular matrix components by trabecular meshwork cells: Possible consequence on aqueous outflow.
小梁网细胞过度合成细胞外基质成分可能影响房水流出
作者：Tane N, Dhar S, Roy S, Pinheiro A, Ohira A, Roy S.
作者单位：Department of Medicine, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA; Department of Ophthalmology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA; Department of Ophthalmology, Shimane University Faculty of Medicine, 89-1, Enya, Izumo, Shimane, 693-8501, Japan.
文摘：The extracellular matrix (ECM) of the trabecular meshwork (TM) is an important determinant of its functional properties.
由小梁网细胞合成的细胞外基质在小梁细胞功能的发挥中起着决定性作用。
This study was performed to investigate whether overexpression of ECM components, laminin (LM) and collagen type IV (Col) by TM cells may play a role in the development of outflow resistance.
实验目的：研究小梁细胞合成的细胞外基质成分层粘连蛋白和IV型胶原是否影响房水流出阻力的形成。
To determine the effect of excess LM and Col expression on cell monolayer permeability, an in vitro cell culture model was used in which overexpression of the two ECM components, LM and Col, was induced by high glucose (HG) (30mM) or 0.1muM dexamethasone (D) in bovine and human trabecular meshwork (BTM and HTM) cells.
为了了解过多的层粘连蛋白和IV型胶原对细胞通透性的影响，我们建立如下体外培养的细胞模型：将高浓度的葡萄糖（30mM）或0.1muM的地塞米松作用于牛眼和人眼的小梁细胞，使其过度表达层粘连蛋白和IV型胶原。
Western blot analysis and immunofluorescence staining confirmed increased LM and Col synthesis in cells exposed to HG or D. Increased level of LM and Col protein resulted in reduced cell monolayer permeability.
蛋白印迹分析和免疫荧光染色显示：葡萄糖或地塞米松促使小梁细胞层粘连蛋白和IV型胶原的表达增加。高水平的层粘连蛋白和IV型胶原使细胞的通透性减低。
Transfection with antisense oligos (AS-oligos) targeted against LM or Col inhibited HG- or D-induced LM and Col gene overexpression in TM cells with concomitant increase in permeability.
将AS-oligo转染小梁细胞后可抑制葡萄糖或地塞米松诱导的小梁细胞层粘连蛋白和IV型胶原的基因表达，细胞的通透性也随之增强。
The AS-oligo strategy was effective in reducing LM or Col level in the TM cells in all conditions tested in this study.
本实验显示在所有的条件下转染AS-oligo技术都可有效的减少小梁细胞层粘连蛋白和IV型胶原的表达。
These findings suggest that increased LM and Col deposition in the outflow pathway may cause resistance to aqueous outflow and contribute to the development of primary open angle glaucoma (POAG).
提示：层粘连蛋白和IV型胶原在房水流出途径中过多的沉积可能引起房水流出阻力增加，在原发性开角性青光眼的发展中可能起到一定的作用。
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作者:admin@医学,生命科学 2010-10-08 17:11
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