scholarly journals Effects of Salidroside on Trabecular Meshwork Cell Extracellular Matrix Expression and Mouse Intraocular Pressure

2019 ◽  
Vol 60 (6) ◽  
pp. 2072 ◽  
Author(s):  
Yuchen Fan ◽  
Li Guo ◽  
Jiahong Wei ◽  
Junzhao Chen ◽  
Hao Sun ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Intraocular Pressure ◽  
Trabecular Meshwork ◽  
Trabecular Meshwork Cell ◽  
Matrix Expression

scholarly journals SNHG3 cooperates with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in human trabecular meshwork cells under oxidative stress

2020 ◽  
Author(s):  
Sizhen Li ◽  
Qingsong Yang ◽  
Zixiu Zhou ◽  
Min Fu ◽  
Xiaodong Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Intraocular Pressure ◽  
Oxidative Damage ◽  
Trabecular Meshwork ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Quantitative Polymerase Chain Reaction ◽  
Subcellular Fractionation ◽  
Cell Counting

Abstract Background: Glaucoma is the main reason for irreversible blindness, and pathological increased intraocular pressure is the leading risk factor for glaucoma. It is reported that trabecular meshwork cell injury is closely associated with the elevated intraocular pressure. The current study aimed to investigate the role of SNHG3 in human trabecular meshwork (HTM) cells under oxidative stress. Methods: A series of experiments including real-time quantitative polymerase chain reaction (RT-qPCR), subcellular fractionation assay, western blot analysis, cell counting kit-8 (CCK-8) assay, RNA pull down, flow cytometry analysis, and RIP assay were employed to explore the biological function and regulatory mechanism of SNHG3 in HTM cells under oxidative stress.Results: First, we observed that H2O2 induced SNHG3 upregulation in HTM cells. Then, we found that SNHG3 silencing alleviated H2O2-induced oxidative damage in HTM cells. Moreover, SNAI2 knockdown alleviated the oxidative damage induced by H2O2 in HTM cells. Mechanistically, SNHG3 bound with ELAVL2 to stabilize SNAI2. Finally, SNAI2 overexpression counteracted the effect of SNHG3 silencing on H2O2-induced HTM cells. Conclusion: Our results demonstrated that SNHG3 cooperated with ELAVL2 to modulate cell apoptosis and extracellular matrix (ECM) accumulation by stabilizing SNAI2 in HTM cells under oxidative stress.

scholarly journals Fluctuations in Intraocular Pressure Increase the Trabecular Meshwork Extracellular Matrix

2014 ◽  
Vol 33 (4) ◽  
pp. 1215-1224 ◽  
Author(s):  
Huan Zou ◽  
Rongdi Yuan ◽  
Qijun Zheng ◽  
Yan Huo ◽  
Min Lang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Intraocular Pressure ◽  
Trabecular Meshwork ◽  
Pressure Increase

scholarly journals Overexpression of SPARC in Human Trabecular Meshwork Increases Intraocular Pressure and Alters Extracellular Matrix

2013 ◽  
Vol 54 (5) ◽  
pp. 3309 ◽  
Author(s):  
Dong-Jin Oh ◽  
Min Hyung Kang ◽  
Yen Hoong Ooi ◽  
Kyu Ryong Choi ◽  
E. Helene Sage ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Intraocular Pressure ◽  
Trabecular Meshwork

scholarly journals Regulation of Trabecular Meshwork Cell Contraction and Intraocular Pressure by miR-200c

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e51688 ◽  
Author(s):  
Coralia Luna ◽  
Guorong Li ◽  
Jianyong Huang ◽  
Jianming Qiu ◽  
Jing Wu ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Trabecular Meshwork ◽  
Cell Contraction ◽  
Trabecular Meshwork Cell

scholarly journals The Effect of Hyaluronic Acid on MMP-9 Expression in Trabecular Meshwork Cell Culture of Patient with Primary Open Angle Glaucoma

2017 ◽  
Vol 3 (1) ◽  
pp. 38
Author(s):  
Cicih Komariah ◽  
Ma’sum Effendi ◽  
Hidayat Sujuti
Keyword(s):  
Cell Culture ◽  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Trabecular Meshwork ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Open Angle ◽  
Trabecular Meshwork Cell ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

In primary open angle glaucoma, decrease of hyaluronic acid level is related to extracellular matrix deposition of trabecular meshwork. Extracellular matrix deposition will increase humor aqueous outflow resistance which in turn increase the intraocular pressure. MMP-9 as one of matrix metalloproteinase (MMP) family, has a high potency to degrade the extracellular matrix. The expression of MMP-9 can be activated by hyaluronic acid through its binding with CD44 as hyaluronic main receptor. The aim of this research is to determine the effect of hyaluronic acid on MMP-9 expression in trabecular meshwork cell culture of patient with primary open angle glaucoma by immunocytochemical method. Trabecular meshwork cell culture were exposed to hyaluronic acid at four different concentration (0mg/ml, 1 mg/mL, 3 mg/mL, 6 mg/mL). After 24 hours incubated, we find a significant difference of MMP-9 expression between control group and group with hyaluronic acid. There was significant correlation between hyaluronic acid and MMP-9 expression. Hyaluronic acid exposure will increase MMP-9 expression in trabecular meshwork cell culture. This finding suggest that hyaluronic acid can influence the resistance of humor aqueous outflow in trabecular meshwork by up-regulating MMP-9 expression, and therefore will increase extracellular matrix degradation.Key words : hyaluronic acid, primary open angle glaucoma, MMP-9

scholarly journals Cathepsin K Regulates Intraocular Pressure by Modulating Extracellular Matrix Remodeling and Actin-Bundling in the Trabecular Meshwork Outflow Pathway

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2864
Author(s):  
Avinash Soundararajan ◽  
Sachin Anil Ghag ◽  
Sai Supriya Vuda ◽  
Ting Wang ◽  
Padmanabhan Paranji Pattabiraman
Keyword(s):  
Extracellular Matrix ◽  
Intraocular Pressure ◽  
Actin Cytoskeleton ◽  
Trabecular Meshwork ◽  
Critical Role ◽  
Constitutive Expression ◽  
Cathepsin K ◽  
Actin Dynamics ◽  
Actin Depolymerization ◽  
Outflow Pathway

The homeostasis of extracellular matrix (ECM) and actin dynamics in the trabecular meshwork (TM) outflow pathway plays a critical role in intraocular pressure (IOP) regulation. We studied the role of cathepsin K (CTSK), a lysosomal cysteine protease and a potent collagenase, on ECM modulation and actin cytoskeleton rearrangements in the TM outflow pathway and the regulation of IOP. Initially, we found that CTSK was negatively regulated by pathological stressors known to elevate IOP. Further, inactivating CTSK using balicatib, a pharmacological cell-permeable inhibitor of CTSK, resulted in IOP elevation due to increased levels and excessive deposition of ECM-like collagen-1A in the TM outflow pathway. The loss of CTSK activity resulted in actin-bundling via fascin and vinculin reorganization and by inhibiting actin depolymerization via phospho-cofilin. Contrarily, constitutive expression of CTSK decreased ECM and increased actin depolymerization by decreasing phospho-cofilin, negatively regulated the availability of active TGFβ2, and reduced the levels of alpha-smooth muscle actin (αSMA), indicating an antifibrotic action of CTSK. In conclusion, these observations, for the first time, demonstrate the significance of CTSK in IOP regulation by maintaining the ECM homeostasis and actin cytoskeleton-mediated contractile properties of the TM outflow pathway.

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