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Autophagy the key player in trabecular meshwork death-mechanistic difference in early and advanced glaucoma

ABSTRACT: This study highlights the differential roles of apoptosis versus autophagy in cell death mechanism in the trabecular meshwork in primary adult glaucoma at various stages. This reflects the possible role of autophagy in causing glaucomatous damage in severe disease stages

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Eye, Eye Trabecular Meshwork

DISEASE(S): Glaucoma

SUBMITTER: gagan jhingan

LAB HEAD: Aparna Rao

PROVIDER: PXD010752 | Pride | 2021-09-08

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	LVPRASAD_TRABMESH.msf	Msf
	Sample_37_POAG1.raw	Raw
	Sample_38_POAG2.raw	Raw
	Sample_39_POAG3.raw	Raw
	Sample_40_PACG1.raw	Raw

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Publications

Switch to Autophagy the Key Mechanism for Trabecular Meshwork Death in Severe Glaucoma.

Rao Aparna A Sahay Prity P Chakraborty Munmun M Prusty Birendra Kumar BK Srinivasan Sandhya S Jhingan Gagan Deep GD Mishra Pragyan P Modak Rahul R Suar Mrutyunjay M

Clinical ophthalmology (Auckland, N.Z.) 20210714

<h4>Purpose</h4>The key differences in cell death mechanisms in the trabecular meshwork (TM) in adult moderate and severe primary glaucoma remain still unanswered. This study explored key differences in cell death mechanisms in the trabecular meshwork (TM) in adult moderate and severe primary glaucoma.<h4>Design</h4>In-vitro laboratory study on surgical specimens and primary cell lines.<h4>Methods</h4>Select cell death-related proteins differentially expressed on mass spectrometric analysis in e ...[more]

PMID: 34285469

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Global and comparative proteome signatures in the lens capsule, trabecular meshwork, and iris of patients with pseudoexfoliation glaucoma

Project description:Pseudoexfoliation (PXF) is characterized by the accumulation of exfoliative material in the eye and high rates of blindness, if left untreated. Pseudoexfoliation glaucoma (PXG) is generally diagnosed too late due to its asymptomatic nature, necessitating the development of new effective screening tools for the early diagnosis of the disease. Thus, the increasing prevalence of this disease due to an aging population has necessitated the identification of suitable biomarkers for the early detection of the disease or detection of the onset of glaucoma in eyes with PXF. We applied a proteomics strategy based on a high-throughput screening method for the determination of proteins involving PXF and PXG pathogenesis. Lens capsule (LC) samples were obtained from surgical trabeculectomy of 146 adults with PXF, PXG, and controls to characterize the proteome profile. Peptides from LC were analyzed using liquid chromatography with tandem mass spectrometry (LC-MS/MS). The protein of interest and cytokines/chemokines profiles were verified using immunohistochemistry and bio-plex kit assay, respectively. We have also analyzed the proteomic profile of trabecular meshwork (TM) and iris samples with PXG compared to control. There were 1433 proteins identified in human LC, of which 27 proteins were overexpressed and 8 proteins were under-expressed in PXG compared with PXF. Overexpressed proteins such as fibromodulin, decorin, lysyl oxidase homolog 1, Collagen alpha-1(I) chain, and Collagen alpha-3(VI) chain were the major components of the extracellular matrix (ECM) proteins involved in cell-matrix interactions or ECM proteoglycans, assembly and crosslinking of collagen fibrils. The ECM composition and homeostasis are altered in glaucoma; thus, quantitative proteomics is a method to discover molecular markers in the eye. Monitoring of these events can help evaluate disease progression in future studies.

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Trabecular meshwork cell-derived exosomal microRNA expression

Project description:Trabecular meshwork cells in eyes with glaucoma aquire mesenchymal phenotypes. The types of microRNAs in exosomes may differ between static and glaucomatous status and their effects on aqueous humor regulation are still uknown. We used microarrays to identify the differential microRNA expression related to interaction between trabecular meshwork cells and Schlemm's canal endothelial cells.

2021-11-17 | GSE175464 | GEO

Effects of dexamethasone for primary trabecular meshwork cell gene expression

Project description:To clarify the effects of dexamethasone treatment for primary trabecular meshwork cell gene expression, which may relates to the pathophysiology of glucocorticoid-induced glaucoma Three lots (lot #2584, 3423 and 4973) of primary culture human trabecular meshwork (TM) cells were purchased from ScienCell Research Laboratories (Carlsbad, CA). The TM cells were treated with and without 100nM dexamethasone (DEX) for 14 days. Genomewide gene expression analysis was carried out using Agilent 8X60K array.

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Transcription profiling by array of human trabecular meshwork cells to investigate the molecular mechanisms by which MYOC mutants cause glaucoma

Project description:Comparison of human trabecular meshwork transcriptomes of cells glaucoma-linked MYOC mutant Q368X

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Comparison of extracellular vesicle proteome between glaucoma and non-glaucoma trabecular meshwork cells

Project description:Extracellular matrix (ECM) materials accumulate in the trabecular meshwork (TM) tissue of patients with glaucoma, which is associated with a decrease in aqueous humor outflow and therefore an increase in intraocular pressure. To explore a potential mechanism for ECM regulation in the TM, we purified extracellular vesicles (EVs) from conditioned media of differentiated TM cells in culture isolated from non-glaucomatous and glaucomatous human donor eyes. EVs were purified using the double cushion ultracentrifugation gradient method. Fractions containing EV markers CD9 and TSG101 were analyzed using nanoparticle tracking analysis to determine their size and concentration. We then determined their proteomic cargo by mass spectrometry and compared protein profiles of EVs between normal and glaucomatous TM cells using PANTHER. Key protein components from EV preparations were validated with Western blotting. Results showed changes in the percentage of ECM proteins associated with EVs from glaucomatous TM cells compared to non-glaucomatous TM cells (5.7% vs 13.1% respectively). Correspondingly, we found that two ECM-related cargo proteins found across all samples, fibronection and EDIL3 were significantly less abundant in glaucomatous EVs (<0.3 fold change across all groups) compared to non-glaucomatous EVs. Overall, these data establish that ECM materials are prominent cargo in EVs from TM cells, and their binding to EVs is diminished in glaucoma

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Dexamethasone induced gene expression changes in the human trabecular meshwork

Project description:One of the undesirable side effects of glucocorticoid use is the potential development of elevated intraocular pressure and glaucoma. The precise mechanisms through which steroid use induces ocular hypertension are unclear. The purpose of this study was to identify gene expression changes induced by steroids in the human trabecular meshwork and the underlying sclerocorneal tissue. The anterior segment of five pairs of adult human donor eyes were maintained in a profusion organ culture system.

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Transcription profiling of human trabecular meshwork cells after TGF-beta1 and 2 treatment

Project description:TGF-beta levels are known to increase in the aqueous humor of eye cells in patients with glaucoma. Increase TGF-beta is assumed to have a biochemical impact on the trabecular meshwork, and an increase in extracellular matrix formation, which may be responsible for decrease outflow facility of the eye. This may increase extracellular pressure, causing glaucoma. TGF-beta 1 may be the cause of abnormal accumulation of extracellular matrices in trabecular meshwork of eyes with primary open angle glaucoma. Transforming growth factor (TGF)-beta2 regulates the expression of proteoglycans in aqueous humor from human glaucomatous eyes. To identify gene expression changes as a result of TGF-beta1 and 2 treatment of human trabecular meshwork cells. We expect to see a change in expression of the proteoglycans in HTM cells as a response to TGF-beta treatment. Human Trabecular Meswork cells in the eye were bathed by aqueous humor. TM cells were removed from individuals with the following ages: 16,66,67,73, and 76. Each individual was treated with EtOH (control), TGF-beta1, or TGF-beta2. Total RNA from each individual was pooled for each chip. Technical replicates were created for each treatment type, for a total of 6 chips.

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TGF-beta1 and 2 treatment of human trabecular meshwork cells (Russell-3U24NS043571-01S1-2)

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