Permissive Effect of Fibronectin on Collagen Gel Contraction Mediated by Bovine Trabecular Meshwork Cells

2003 ◽  
Vol 44 (10) ◽  
pp. 4331 ◽  
Author(s):  
Yoshikuni Nakamura ◽  
Takeshi Sagara ◽  
Keisuke Seki ◽  
Shinji Hirano ◽  
Teruo Nishida
Keyword(s):  
Trabecular Meshwork ◽  
Collagen Gel ◽  
Trabecular Meshwork Cells ◽  
Collagen Gel Contraction

scholarly journals Functional Implications of Cross-Linked Actin Networks in Trabecular Meshwork Cells

2018 ◽  
Vol 45 (2) ◽  
pp. 783-794 ◽  
Author(s):  
Laura Duffy ◽  
Steven O’Reilly
Keyword(s):  
Trabecular Meshwork ◽  
Open Angle Glaucoma ◽  
Collagen Gel ◽  
Mechanical Stretch ◽  
Actin Networks ◽  
Trabecular Meshwork Cells ◽  
Microscopy Technique ◽  
Collagen Gel Contraction

Background/Aims: The Trabecular meshwork (TM) is the tissue responsible for outflow resistance and therefore intraocular pressure. TM cells contain a contractile apparatus that is composed of actin stress fibres which run parallel to the axis of the cell and are responsible for facilitating contraction. Cross-Linked Actin Networks (CLANs) are polygonal arrangements of actin that form a geodesic network found predominantly in TM cells both in situ and in vitro. The aim of this work is to determine the functional significance of CLANs in TM cells and to assess the effect of mechanical stretch stimulation on the induction (or not) of CLANs. Methods: We used collagen gel contraction models to demonstrate functional impairment of cells when induced to express CLANs in situ. Cyclic mechanical stretch was used to stimulate cells and measure CLANs Results: CLANs inhibited contraction and cyclic mechanical stretch induced CLANs. Furthermore, we also demonstrated that using shape alone we could predict the appearance of CLANs using a simple light microscopy technique. Conclusion: Taken together we have now shown, for the first time, a functional deficit In TM cells with CLANs Furthermore that shape alone can predict the appearance of CLAN containing cells. CLANs can now be linked to a functional effect and may underlie the appearance of CLANs with the pathology of primary open angle glaucoma (POAG).

Mechanical stretch upregulates connexin43 in human trabecular meshwork cells

2019 ◽  
Author(s):  
Nikoleta Tellios ◽  
Mary Feng ◽  
Nancy Chen ◽  
Hong Liu ◽  
Vasiliki Tellios ◽  
...  
Keyword(s):  
Trabecular Meshwork ◽  
Mechanical Stretch ◽  
Trabecular Meshwork Cells

Effect of dexamethasone on the expression of MMPs, adenosine A1 receptors and NFKB by human trabecular meshwork cells

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Normie Aida Mohd Nasir ◽  
Renu Agarwal ◽  
Anna Krasilnikova ◽  
Siti Hamimah Sheikh Abdul Kadir ◽  
Igor Iezhitsa
Keyword(s):  
Extracellular Matrix ◽  
Western Blot ◽  
Trabecular Meshwork ◽  
Culture Media ◽  
Smooth Muscle Actin ◽  
Adenosine A1 Receptors ◽  
Trabecular Meshwork Cells ◽  
Aqueous Humor Dynamics ◽  
Nfkb Activation ◽  
Adenosine A1

AbstractObjectivesSteroid-induced ocular hypertension and glaucoma are associated with extracellular matrix remodeling at the trabecular meshwork (TM) of the eye due to reduced secretion of matrix metalloproteinases (MMPs), a family of enzymes regulating extracellular matrix proteolysis. Several biological functions of steroids are known to involve regulation of adenosine A1 receptors (A1AR) and nuclear factor kappa B (NFKB). Since MMPs expression in TM has been shown to be regulated by A1AR as well as transcription factors, it is likely that dexamethasone-induced changes in aqueous humor dynamics involve reduced MMP and A1AR expression and reduced NFKB activation. Hence, the current study investigated the association of dexamethasone-induced reduction in MMP secretion with reduced NFKB activation and A1AR expression.MethodsHuman trabecular meshwork cells (HTMCs) were characterized by estimating myocilin and alpha smooth muscle actin expression and then were treated with dexamethasone 100 nM for 2, 5 and 7 days. The MMP secretion was estimated in culture media using Western blot. Immunocytochemistry (ICC) and ELISA were done to investigate the effect of dexamethasone on NFKB phosphorylation. A1AR expression in HTMCs was determined using Western blot and ELISA.ResultsDexamethasone caused a significant reduction in both MMP-2 and -9 expression compared to untreated group after five and seven days but not after two days of culture. Significantly reduced phosphorylated NFKB and A1AR protein levels were detected in dexamethasone treated compared to vehicle treated HTMCs after five days of culture.ConclusionsDexamethasone reduces MMP-2 and -9 secretion by HTMCs and this effect of dexamethasone is associated with reduced NFKB phosphorylation and A1AR expression.

scholarly journals Cathepsin B Localizes in the Caveolae and Participates in the Proteolytic Cascade in Trabecular Meshwork Cells. Potential New Drug Target for the Treatment of Glaucoma

2020 ◽  
Vol 10 (1) ◽  
pp. 78
Author(s):  
April Nettesheim ◽  
Myoung Sup Shim ◽  
Angela Dixon ◽  
Urmimala Raychaudhuri ◽  
Haiyan Gong ◽  
...  
Keyword(s):  
Trabecular Meshwork ◽  
Cathepsin B ◽  
Molecular Mechanisms ◽  
Culture Media ◽  
Ecm Remodeling ◽  
Trabecular Meshwork Cells ◽  
Proteolytic Cascade

Extracellular matrix (ECM) deposition in the trabecular meshwork (TM) is one of the hallmarks of glaucoma, a group of human diseases and leading cause of permanent blindness. The molecular mechanisms underlying ECM deposition in the glaucomatous TM are not known, but it is presumed to be a consequence of excessive synthesis of ECM components, decreased proteolytic degradation, or both. Targeting ECM deposition might represent a therapeutic approach to restore outflow facility in glaucoma. Previous work conducted in our laboratory identified the lysosomal enzyme cathepsin B (CTSB) to be expressed on the cellular surface and to be secreted into the culture media in trabecular meshwork (TM) cells. Here, we further investigated the role of CTSB on ECM remodeling and outflow physiology in vitro and in CSTBko mice. Our results indicate that CTSB localizes in the caveolae and participates in the pericellular degradation of ECM in TM cells. We also report here a novel role of CTSB in regulating the expression of PAI-1 and TGFβ/Smad signaling in TM cells vitro and in vivo in CTSBko mice. We propose enhancing CTSB activity as a novel therapeutic target to attenuate fibrosis and ECM deposition in the glaucomatous outflow pathway.

Elasticity-Dependent Modulation of TGF-β Responses in Human Trabecular Meshwork Cells

2011 ◽  
Vol 52 (6) ◽  
pp. 2889 ◽  
Author(s):  
Hong Han ◽  
Thomas Wecker ◽  
Franz Grehn ◽  
Günther Schlunck
Keyword(s):  
Trabecular Meshwork ◽  
Trabecular Meshwork Cells

Primary Trabecular Meshwork Cells Incubated in Human Aqueous Humor Differ from Cells Incubated in Serum Supplements

2005 ◽  
Vol 46 (8) ◽  
pp. 2848 ◽  
Author(s):  
Michael P. Fautsch ◽  
Kyle G. Howell ◽  
Anne M. Vrabel ◽  
M. Cristine Charlesworth ◽  
David C. Muddiman ◽  
...  
Keyword(s):  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Trabecular Meshwork Cells
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