Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Delay of Diabetic Cataract Progression by a Chemical Chaperone Trimethylamine N-Oxide through Alleviating Unfolded-Protein-Induced ER Stress

ABSTRACT: Diabetic cataract (DC), characterized by lens cloudiness, is a leading cause of visual impairment in diabetic individulas. This study aims to investigate the protective effects of trimethylamine N-oxide (TMAO), a natural occurring chaperone, on delaying diabetic cataract (DC) progression. In vivo and ex vivo, TMAO reduced high glucose (HG)-induced lens opacity and EMT in rat lens epithelial cells (LECs). In vitro experiments demonstrated that HG resulted in enhanced apoptosis, migration, ROS and EMT-related genes in HLE-B3 cells while TMAO addition diminished these effects. RNA-seq revealed that the inhibition of ER stress was the key factor to reverse the impacts of HG on LECs by TMAO and mechanistic investigations suggested that ER stress-related pathway were significantly inhibited in TMAO treated LECs under HG or tunicamycin-induced ER stress. Moreover, TMAO improved the solubility of lens protein in DC rats. Our study pioneered the confirmation of the protective role of TMAO in DC through inhibiting lens protein unfolding, suppressing ER stress, and alleviating ER stress-induced apoptosis, ROS and EMT in LECs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE338786 | GEO | 2026/09/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Upregulation of N6-methyladenosine Transcript Landscape in Diabetic Cataract

Project description:Epitranscriptomic profiling of human LECs of DC patients comparing normal control LECs. Goal was todetermine the potential functions and mechanism of N6-methyladenosine (m6A) abnormality of RNAs in human lens epithelium cell (HLEC) lesions in diabetic cataract (DC).

2025-02-22 | GSE197371 | GEO

SH2B1 Promotes Apoptosis in Diabetic Cataract via p38 MAPK Pathway

Project description:Diabetic patients face an increased risk of developing cataracts, with unclear mechanisms. Our study illuminates these mechanisms by identifying differentially expressed proteins in the lens anterior capsule of diabetic cataract (DC) and age-related cataract patients using quantitative proteomics. We found SH2B1 to be crucial in DC progression. Reduced SH2B1 expression was confirmed through PCR and Western blotting in patient samples, diet-induced obese mice, and high-glucose (HG)-cultured human lens epithelial cells. Under HG conditions, cell proliferation decreased, while migration and apoptosis, alongside changes in Bcl2 and caspase 3 expression, increased. Overexpressing SH2B1 alleviated these changes and influenced the p38 MAPK signaling pathway. This suggests SH2B1 and the p38 MAPK pathway as significant in DC pathogenesis and potential therapeutic targets. Clinically, this could lead to therapies aimed at halting or slowing DC progression.

2025-05-07 | PXD059243 | Pride

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [mouse_ASC]

Project description:Purpose: TGF-β/BMP signaling pathway has a significant role in fibrotic cataract. Smurf1, a ubiquitin protein ligase, regulates the TGF-β/BMP signaling pathway through the ubiquitin-proteasome system (UPS). This study aims to investigate the role of Smurf1 in the progression of fibrotic cataract and its underlying mechanism.Method: We employed a mouse injury-induced anterior subcapsular cataract (ASC) model and administered Smurf1 inhibitor A01 through anterior chamber injection for in vivo investigation. RNA sequencing was performed to examine global gene expression changes. The volume of the subcapsular opacity was determined using whole-mount immunofluorescence of lens anterior capsules. Lentivirus was utilized to create cell lines with Smurf1 knockdown or overexpression in SRA01/04. Protein levels were assessed by Simple Western. Lens epithelial cell (LEC) proliferation was evaluated by CCK8 and EdU assays. LEC migration was measured by Transwell and wound healing assays.Results: The mRNA levels of genes associated with cell proliferation, migration, epithelial-mesenchymal transition (EMT), TGF-β/BMP pathway and UPS, including Smurf1, were upregulated in ASC model. The mRNA expression of Smurf1 was also upregulated in anterior lens capsules of age-related cataract patients. Anterior chamber injection of A01 inhibited ASC formation and EMT. In vitro knockdown of Smurf1 resulted in reduced proliferation, TGF-β2-induced migration and EMT of LECs. Smurf1 inhibition upregulated Smad1, Smad5 and pSmad1/5. Conversely, Smurf1 overexpression displayed the opposite phenotypes.Conclusion: Smurf1 regulated the progression of fibrotic cataract by influencing the proliferation, migration and EMT of LECs through regulation of Smad signaling pathway, offering a novel target for the treatment of fibrotic cataract.

2024-02-14 | GSE245411 | GEO

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [cell line]

2024-02-14 | GSE245407 | GEO

RNA-seq Analysis of Human Lens Capsules from Donors with and without Cataract Surgery History

Project description:Cataract surgery is the most commonly performed ophthalmic procedure worldwide, yet the long-term molecular adaptations of lens epithelial cells (LECs) following surgery remain poorly understood. In this study, we conducted bulk RNA sequencing on lens capsules from 34 human donors, including 17 with an average of 7 years post-cataract surgery and 17 non-cataract controls. Differential expression analysis revealed substantial transcriptional changes in post-surgical LECs, including 1,690 upregulated and 579 downregulated genes. Gene Set Enrichment Analysis (GSEA) and Gene Ontology (GO) analyses identified activation of oxidative stress response, cell survival pathways, and immune response signatures. Collectively, our findings reveal that LECs undergo profound and sustained molecular reprogramming following cataract surgery, including inflammatory, fibrotic, migratory, and senescent changes. These adaptations may contribute to posterior capsule opacification (PCO) and highlight potential therapeutic targets for its prevention.

2025-07-23 | GSE295383 | GEO

Expression data from rat lens epithelial cells after extracapsular lens extraction (ECLE)

Project description:The epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) has been proposed as a major cause of posterior capsule opacification (PCO) after cataract surgery. Molecular mechanism of PCO progression is still unclear. Using a microarray-based approach, herein we studied the changes in gene expression pattern during rat PCO formation in vivo as a model.

2020-09-30 | GSE152593 | GEO

Proteomic analysis of healthy human Aqueous Humour, Anterior Lens Capsules, and Crystalline Lenses

Project description:Participants were recruited from the Ophthalmology Department among patients scheduled for cataract surgery. Patients were stratified into four distinct groups based on their clinical profiles. ARC group (Age-Related Cataract) included individuals over the age of 75 without a history of diabetes; DC group (Diabetic cataract) included individuals un-der the age of 65 with a known diagnosis of type 1 or type 2 diabetes mellitus; PVC group (Post-Vitrectomy cataract) included individuals of any age, without diabetes, who had undergone vitrectomy with gas tamponade for retinal detachment within the previous 12 months and who had clear lens prior to vitrectomy; and the control group included indi-viduals under the age of 60, without diabetes, who underwent clear lens extraction for re-fractive reasons.

2025-12-01 | PXD069667 | Pride

Autophagy facilitates age-related cell apoptosis - a new insight from senile cataract

Project description:Age-related cell loss underpins many senescence-associated diseases. Senile cataract is a primary blindness-causing age-related ocular disease. Apoptosis of lens epithelial cells (LECs) is the common cellular basis of senile cataract resulted from prolonged exposure to oxidative stress, the mechanism of which remains elusive. Here we reported the concomitance of increased autophagy and apoptosis in the same LEC from senile cataract patients. Oxidative stress triggered autophagy preceded apoptosis, while blocking autophagy by ablation of Atg7 or Atg3 gene remarkably suppressed apoptosis in HLE-B3 cell line. We identified autophagy adaptor SQSTM1/p62 as the critical scaffold protein to sustain a pro-survival signaling PKCι-NF-κB cascades, which antagonized the pro-apoptotic signaling in LECs. Importantly, prolonged autophagy in human senescent LECs responding to oxidative stress induced extensive degradation of p62 protein and therefore facilitated apoptosis. Moreover, pharmacological inhibitor of autophagy, 3-MA, significantly rescued apoptosis of human senescent LECs challenged by oxidative stress. Collectively, our data demonstrated that hyperactivation of autophagy aggravates age-related apoptotic cell death via inhibiting the p62-PKCι-NF-κB pro-survival axis in human senescent LECs. This work expands the understanding of the etiology of senile cataract and provides insight for mechanisms of age-related cell death in senescence-associated diseases.

2022-01-19 | GSE161701 | GEO

Transcriptomic changes in lens epithelial cells at 72 hours post cataract surgery

Project description:This trancriptomic analysis describes the gene expression changes observed in wildtype lens epithelial cells (LECs) by 72 hours compared to zero hours post cataract surgery

2025-08-05 | GSE267060 | GEO

Transcriptomic changes in lens epithelial cells at 5 days post cataract surgery

Project description:This trancriptomic analysis describes the gene expression changes observed in wildtype lens epithelial cells (LECs) by 5 days compared to zero hours post cataract surgery

2025-08-05 | GSE266635 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data