scholarly journals Down-regulation of 14-3-3 Zeta Inhibits TGF-β1–Induced Actomyosin Contraction in Human Trabecular Meshwork Cells Through RhoA Signaling Pathway

2016 ◽  
Vol 57 (2) ◽  
pp. 719 ◽  
Author(s):  
Yiming Ye ◽  
Yangfan Yang ◽  
Xiaoxiao Cai ◽  
Liling Liu ◽  
Kaili Wu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Trabecular Meshwork ◽  
Down Regulation ◽  
Trabecular Meshwork Cells ◽  
Rhoa Signaling ◽  
Actomyosin Contraction ◽  
Tgf Β1

scholarly journals Inhibition of RhoA Signaling with Increased Bves in Trabecular Meshwork Cells

2010 ◽  
Vol 51 (1) ◽  
pp. 223 ◽  
Author(s):  
Patricia K. Russ ◽  
Asher I. Kupperman ◽  
Sai-Han Presley ◽  
Frederick R. Haselton ◽  
Min S. Chang
Keyword(s):  
Trabecular Meshwork ◽  
Trabecular Meshwork Cells ◽  
Rhoa Signaling

scholarly journals miR-136 improves renal fibrosis in diabetic rats by targeting down-regulation of tyrosine kinase SYK and inhibition of TGF-β1/Smad3 signaling pathway

Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 513-522 ◽  
Author(s):  
Lei Liu ◽  
Xinlu Pang ◽  
Wenjun Shang ◽  
Guiwen Feng ◽  
Zhigang Wang ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Diabetic Rats ◽  
Down Regulation ◽  
Tgf Β1

scholarly journals Effect of Elevated Intracellular cAMP Levels on Actomyosin Contraction in Bovine Trabecular Meshwork Cells

2011 ◽  
Vol 52 (3) ◽  
pp. 1474 ◽  
Author(s):  
Charanya Ramachandran ◽  
Rajkumar V. Patil ◽  
Najam A. Sharif ◽  
Sangly P. Srinivas
Keyword(s):  
Trabecular Meshwork ◽  
Intracellular Camp ◽  
Trabecular Meshwork Cells ◽  
Actomyosin Contraction ◽  
Camp Levels

Effects of hyperglycemia on the TGF-β pathway in trabecular meshwork cells

2021 ◽  
Author(s):  
Hsin-Yi Chen ◽  
Mei-Lan Ko ◽  
Hong-Lin Chan
Keyword(s):  
Oxidative Stress ◽  
Signal Transduction ◽  
Protein Expression ◽  
Trabecular Meshwork ◽  
Calcium Release ◽  
Cell Function ◽  
Vascular Complications ◽  
Inflammasome Activation ◽  
Trabecular Meshwork Cells ◽  
Tgf Β1

Abstract Background: Hyperglycemia, which can lead to apoptosis, hypertrophy, and fibrosis, induces hyperinflammation through inflammasome activation. A major cause of diabetic vascular complications is increased oxidative stress due to hyperglycemia. In order to elucidate the potential dual roles and regulatory signal transduction of TGF-β1 and TGF-β2 in human trabecular meshwork cells (HTMCs) in vitro, we established an oxidative cell model in HTMCs using 5.5, 25, 50, and 100 mM D-glucose-supplemented media and characterized the TGF-β-related oxidative stress pathway. Methods: Further analysis was conducted to investigate oxidative damage and protein alterations in the trabecular meshwork caused by the signal transduction. This was done through a series of qualitative cell function studies, such as cell viability/apoptosis analysis, intracellular reactive oxygen species (ROS) detection, analysis of calcium release concentration, immunoblot analysis to detect the related protein expression alteration, and analysis of cell fibrosis to study the effect of different severities of hyperglycemia. We also illustrated the role of TGF-β1 and TGF-β2 in oxidative stress-induced injury by shRNA-mediated knockdown or stimulation with recombinant human TGF-β1 protein (rhTGF-β1). Results: Results from the protein expression analysis showed that p-JNK, p-p38, p-AKT, TGF-β1, TGF-β2, and related SMAD family members were upregulated in HTMCs under hyperglycemia. In the cell functional assays, HTMCs treated with rhTGFβ-1 (1 ng/mL) and under hyperglycemic conditions showed higher proliferation rates and lower ROS and calcium levels than those with higher concentration or without rhTGFβ-1 treated. Furthermore, TGF-β1 and TGF-β2 were found to be associated with the activation of fibrosis-response proteins, α-SMA, collagen I, and laminin, which may lead to HTMC damage. Conclusions: To summarize, mechanistic analyses in HTMCs showed that hyperglycemia-induced oxidative stress activated TGF-β1 along with its associated pathway: at low concentrations, TGF-β1 protects cells from antioxidation, whereas at high concentrations, it accumulates in the extracellular matrix, causing further HTMC dysfunction.

scholarly journals Prostaglandin EP2 receptor signaling protects human trabecular meshwork cells from apoptosis induced by ER stress through down-regulation of p53

2016 ◽  
Vol 1863 (9) ◽  
pp. 2322-2332 ◽  
Author(s):  
Georges Kalouche ◽  
Céline Boucher ◽  
Annick Coste ◽  
Laurent Debussche ◽  
Cécile Orsini ◽  
...  
Keyword(s):  
Er Stress ◽  
Trabecular Meshwork ◽  
Receptor Signaling ◽  
Down Regulation ◽  
Trabecular Meshwork Cells ◽  
Ep2 Receptor

scholarly journals Suppression of TGF-β1 signaling by Matrigel via FAK signaling in cultured human trabecular meshwork cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuan Zhang ◽  
Scheffer C. G. Tseng ◽  
Ying-Ting Zhu
Keyword(s):  
Extracellular Matrix ◽  
Trabecular Meshwork ◽  
Culture System ◽  
Physiological Role ◽  
Active Role ◽  
Outflow Resistance ◽  
Trabecular Meshwork Cells ◽  
Gradual Loss ◽  
Shed Light ◽  
Tgf Β1

AbstractThe trabecular meshwork (TM) is composed of TM cells and beams of the extracellular matrix, together contributing to aqueous humor (AH) outflow resistance. Herein, we validated that our culture system on 2D Matrigel expressed putative TM markers and myocilin, of which the latter was upregulated by dexamethasone. Continuous passage of these cells on 2D Matrigel resulted in a gradual loss of expression of these markers. However, such a loss was restored by seeding cells in 3D Matrigel where expression of TM markers was further upregulated upon continuous passage. In contrast, TM cells seeded on fibronectin, collagen I/IV, or laminin lost expression of these markers and turned into myofibroblasts with expression of αSMA, which were dose-dependently upregulated by TGF-β1/TGF-β2. TM cells in 3D Matrigel also expressed TGF-β1/TGF-β3 despite challenge of TGF-β1. The maintenance of TM phenotype by 3D Matrigel was linked to inhibition of canonical TGF-β signaling and activation of pFAK-pSrc-pP190RhoGAP-P120RasGAP signaling. These findings indicate that basement membrane matrix with low rigidity plays an active role in maintaining TM phenotype in the presence of TGF-β1 and shed light on its physiological role. Furthermore, abnormal matrices may perpetuate the pathological TM phenotype when the level of TGF-β2 is elevated in glaucoma patients.

scholarly journals Characterization of TGF-β by Induced Oxidative Stress in Human Trabecular Meshwork Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 107
Author(s):  
Hsin-Yi Chen ◽  
Hsiu-Chuan Chou ◽  
Yi-Jung Ho ◽  
Shing-Jyh Chang ◽  
En-Chi Liao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Trabecular Meshwork ◽  
Protein Level ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Trabecular Meshwork Cells ◽  
Tgf Β1

Oxidative stress generated by reactive oxygen species (ROS) plays a critical role in the pathomechanism of glaucoma, which is a multifactorial blinding disease that may cause irreversible damage within human trabecular meshwork cells (HTMCs). It is known that the transforming growth factor-β (TGF-β) signaling pathway is an important component of oxidative stress-induced damage related to extracellular matrix (ECM) fibrosis and activates cell antioxidative mechanisms. To elucidate the dual potential roles and regulatory mechanisms of TGF-β in effects on HTMCs, we established an in vitro oxidative model using hydrogen peroxide (H2O2) and further focused on TGF-β-related oxidative stress pathways and the related signal transduction. Via a series of cell functional qualitative analyses to detect related protein level alterations and cell fibrosis status, we illustrated the role of TGF-β1 and TGF-β2 in oxidative stress-induced injury by shTGF-β1 and shTGF-β2 knockdown or added recombinant human TGF-β1 protein (rhTGF-β1). The results of protein level showed that p38 MAPK, TGF-β, and its related SMAD family were activated after H2O2 stimulation. Cell functional assays showed that HTMCs with H2O2 exposure duration had a more irregular actin architecture compared to normal TM cells. Data with rhTGF-β1 (1 ng/mL) pretreatment reduced the cell apoptosis rate and amount of reactive oxygen species (ROS), while it also enhanced survival. Furthermore, TGF-β1 and TGF-β2 in terms of antioxidant signaling were related to the activation of collagen I and laminin, which are fibrosis-response proteins. Succinctly, our study demonstrated that low concentrations of TGF-β1 (1 ng/mL) preserves HTMCs from free radical-mediated injury by p-p38 MAPK level and p-AKT signaling balance, presenting a signaling transduction mechanism of TGF-β1 in HTMC oxidative stress-related therapies.

Trabecular Meshwork Stem Cells Could Be Differentiated to Be Trabecular Meshwork Cells with Secretory Functions

2019 ◽  
Author(s):  
Ying Su ◽  
Xin Jiang ◽  
Elizabeth (Xiaomeng) Wang ◽  
Feng Wang ◽  
Ying Han
Keyword(s):  
Stem Cells ◽  
Trabecular Meshwork ◽  
Trabecular Meshwork Cells

Adrenomedullin Rescues Testicular Steroidogenesis of Leydig Cells by Suppressing TGF-β1 via PI3K/Akt-Dependent Activation of GSK-3β/β-Catenin Signaling Pathway

2020 ◽  
Author(s):  
Wei Hu ◽  
Xia-lian Zhu ◽  
Chang-geng Xu ◽  
Ming-yong Li ◽  
Wei Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Leydig Cells ◽  
Testicular Steroidogenesis ◽  
Gsk 3Β ◽  
Tgf Β1
Sign in / Sign up

Export Citation Format

Share Document