2000
DOI: 10.1006/exer.1999.0764
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The Similarity of Protein Expression in Trabecular Meshwork and Lamina Cribrosa: Implications for Glaucoma

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Cited by 36 publications
(28 citation statements)
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“…9). DISCUSSION iTRAQ-based proteomics analysis enables the investigation of the mechanisms of disease using a multiplexed approach (53,55,57,61,70). This is the first time that the iTRAQ technique has been used to explore optic nerve head glial cell activation, believed to be involved in the very earliest stages of the development of glaucomatous optic neuropathy (7,17).…”
Section: Resultsmentioning
confidence: 99%
“…9). DISCUSSION iTRAQ-based proteomics analysis enables the investigation of the mechanisms of disease using a multiplexed approach (53,55,57,61,70). This is the first time that the iTRAQ technique has been used to explore optic nerve head glial cell activation, believed to be involved in the very earliest stages of the development of glaucomatous optic neuropathy (7,17).…”
Section: Resultsmentioning
confidence: 99%
“…2-4), or H 2 O 2 treatment (Figs. [6][7][8]. Initially, we demonstrated that FG-3019 inhibits CTGF by effecting associated cellular functions such as induction of Erk1/2 phosphorylation previously described to induce fibronectin and CTGF-mediated adhesion/cell spreading 54 ( Fig.…”
Section: Discussionmentioning
confidence: 99%
“…It has been hypothesized that the TM and the LC are biochemically similar tissues and that the cells cultured from the two are very similar. [8][9][10][11][12][13][14][15] Our group and others have previously examined the fibrotic phenotype associated with glaucoma in the LC and TM regions, including increased expression of collagen type 1. 9,15,16 In glaucoma, the LC undergoes thickening 17 and posterior migration 18 in the early stages of the disease process, and later undergoes shearing and collapse of the LC plates finally leading to a thin fibrotic connective tissue structure/scar.…”
mentioning
confidence: 99%
“…Hence mutant myocilin impairs mitochondrial functions in human trabecular meshwork cells (He et al 2009) and may confer different sensitivity to oxidative stress depending on the mutation of this protein (Joe and Tomarev 2010) as induced on genetic basis in juvenile glaucoma or on degenerative ROS-mediated basis in POAG. The presence of neuronal proteins in AH is not surprising, because TM cells have a neuroectodermic origin, expressing, at least in part, a neural-like phenotype (Steely et al 2000) TM cells deriving from mesenchymal cells of the neural crest (Cvekl and Tamm 2004). The role of neural proteins in glaucoma pathogenesis is established.…”
Section: Proteins In Glaucomatous Aqueous Humourmentioning
confidence: 99%