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ABSTRACT:
PROVIDER: PRJNA785074 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: To characterize microRNAs (miRNAs) and their possible roles in high myopia by using next generation sequencing Methods: Aqueous humor samples were obtained from 15 highly myopic eyes and 15 cataract eyes at the onset of surgery. miRNA next generation sequencing and bioinformatics analyses were performed using RNA extracted from aqueous humor samples. Results: A total of 341 miRNAs were detected in the aqueous humor samples of highly myopic eyes; 201 miRNAs were detected in the aqueous humor samples of cataractous control eyes. A total of 249 mature miRNAs and 17 novel miRNAs were differentially expressed during myopia. Possible pathways regulated by these aberrantly expressed miRNAs included the TNF, MAPK, PI3K-Akt, and HIF-1 signaling pathways. Conclusions: The current study provided an overall view of miRNA profiling in the aqueous humor of highly myopic eyes. These profiles may be associated with myopia pathogenesis, and are potential biomarkers.
2021-12-15 | GSE142359 | GEO
Project description:To explore the regulatory mechanism of age-related cataract (ARC) formation and progression，we construct sodium selenite-induced rat cataract model and performed the high-throughput RNA sequencing (HTS) technology to identify the mRNA and miRNA expression profiles of the lens from Na2Se03-induced and saline - injected Sprague Dawley rats.
2023-11-22 | GSE226272 | GEO
Project description:This work describes a proteomic analysis for different types of glaucoma (PACG, NVG) and age-related cataract as control. The AH samples were recruited from 175 individual patients with PACG, NVG and age-related cataract. First, in discovery cohort the AH proteome characteristics of PAACG, PCACG and NVG with cataract were compared by DIA approach. Second, AH proteomic features of three types of glaucoma, PAACG, PCACG and NVG, were mutually compared. In validation cohort the key proteins of above comparison were validated by PRM approach.
2021-08-02 | PXD027686 |
Project description:To explore the regulatory mechanism of age-related cataract (ARC) formation and progression，we construct sodium selenite-induced rat cataract model and performed the high-throughput RNA sequencing (HTS) technology to identify the mRNA and miRNA expression profiles of the lens from Na2Se03-induced and saline - injected Sprague Dawley rats.
2023-11-22 | GSE226273 | GEO
Project description:To characterize the N6-methyladenosine (m6A) modification patterns in long non-coding RNAs (lncRNAs) in sporadic congenital cataract (CC) and age-related cataract(ARC).
2024-11-06 | GSE221970 | GEO
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
Project description:Characterization of N6-Methyladenosine lncRNAs in sporadic congenital cataract and age-related cataract
| PRJNA917038 | ENA
Project description:Transcriptomic analysis of human lens and age-related cataract
| PRJNA881318 | ENA
Project description:Protein post-translational modifications (PTMs) have been associated with aging and age-related diseases. PTMs are particularly impactful in long-lived proteins, such as those found in the ocular lens, because they accumulate with age. Two post-translational modifications that lead to protein-protein crosslinks in aged and cataractous lenses are dehydroalanine (DHA) and dehydrobutyrine (DHB); formed from cysteine/serine and threonine residues, respectively. The purpose of this study was to quantitate DHA and DHB in human lens proteins as a function of age and cataract status. Human lenses of various ages were divided into five donor groups: transparent lenses (18–22-year-old, 48–64-year-old, and 70–93-year-old) and cataractous human lenses of two age groups (48–64-year-old lenses, and 70–93-year-old lenses) and were subjected to proteomic analysis. Relative DHA and DHB peptide levels were quantified and compared to their non-modified peptide counterparts. For most lens proteins containing DHA or DHB, higher amounts of DHA- and DHB-modified peptides were detected in aged and cataractous lenses. DHA-containing peptides were classified into three groups based on abundance changes with age and cataract: those that (1) increased only in age-related nuclear cataract (ARNC), (2) increased in aged and cataractous lenses, and (3) decreased in aged lenses and ARNC. There was no indication that DHA or DHB levels were dependent on lens region. In most donor groups, proteins with DHA and DHB were more likely to be found among urea-insoluble proteins rather than among water- or urea-soluble proteins. DHA and DHB formation may induce structural effects that make proteins less soluble in water that leads to age-related protein insolubility and possibly aggregation and light scattering.
2023-10-12 | PXD045734 | Pride
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