Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [mouse_ASC]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1028297 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26388239_1.fastq.gz | Fastqsanger.gz | |||
| SRR26388239_2.fastq.gz | Fastqsanger.gz | |||
| SRR26388240_1.fastq.gz | Fastqsanger.gz | |||
| SRR26388240_2.fastq.gz | Fastqsanger.gz | |||
| SRR26388241_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
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
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 | GSE245407 | GEO
Project description:Smurf1 modulates Smad signaling pathway in fibrotic cataract formation
| PRJNA1028296 | ENA
Project description:Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [cell line]
| PRJNA1028293 | ENA
Project description:PurposeTGF-β/BMP signaling pathway plays 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.MethodsWe used a mouse model of injury-induced anterior subcapsular cataract (ASC) and administered the Smurf1 inhibitor A01 for in vivo investigations. RNA sequencing was performed to examine global gene expression changes. Protein levels were assessed by Simple Western analysis. The volume of subcapsular opacity was determined using whole-mount immunofluorescence of lens anterior capsules. Lentivirus was utilized to establish cell lines with Smurf1 knockdown or overexpression in SRA01/04. Lens epithelial cell (LEC) proliferation was evaluated by CCK8 and EdU assays. Cell cycle profile was determined by flow cytometry. LEC migration was measured using Transwell and wound healing assays.ResultsThe mRNA levels of genes associated with cell proliferation, migration, epithelial-mesenchymal transition (EMT), TGF-β/BMP pathway, and UPS were upregulated in mouse ASC model. Smurf1 mRNA and protein levels were upregulated in lens capsules of patients and mice with ASC. Anterior chamber injection of A01 inhibited ASC formation and EMT. In vitro, Smurf1 knockdown reduced proliferation, migration and TGF-β2-induced EMT of LECs, concomitant with the upregulation of Smad1, Smad5, and pSmad1/5. Conversely, overexpression of Smurf1 showed opposite phenotypes.ConclusionsSmurf1 regulates fibrotic cataract progression by influencing LEC proliferation, migration, and EMT through the modulation of the Smad signaling pathway, offering a novel target for the fibrotic cataract treatment.
| S-EPMC10854413 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-02-14 | GSE245412 | GEO
Project description:RNAseq analysis was used to determine the transcriptomic changes associated with regenerative vs. fibrotic repair to lens injury. Using an ex vivo post-cataract surgery model, we can follow two distinct outcomes to lens injury: 1) A regenerative wound healing response that ensues across the cell-denuded lens capsule basement membrane (BM), culminating in wound closure on Day 3 (D3) post-injury. 2) Induction of fibrosis, which occurs when a wound healing response occurs off the lens capsule, termed the extracapsular zone (ECZ), where transition to a fibrotic phenotype occurs on day 3 post-injury. Here, we report the changes in the transcriptome that occur on D1, D2, and D3 post-injury, a period that covers wound healing across the BM and time points prior to (D1, D2) and after induction of the fibrotic phenotype (D3). Our data provides a molecular map for understanding the gene changes associated with navigating normal and pathological outcomes to lens injury.
2025-06-02 | GSE298481 | GEO
Project description:We aim to the investigate the role of SMURF1 in breast cancer progression. MCF-7 cells were used as the model and SMURF1 was silenced by siRNA.
2018-08-14 | GSE102653 | GEO
Project description:Transcriptome analysis of RNAs extracted from livers of wild type or Smurf1 knock out (KO) or Smurf2 KO mice at age of 11 month old. We prepared RNA from the following groups: livers of Wild type (WT) or Smurf1 KO or Smurf2 KO mouse from mixed Black Swiss/129SvEv background at age of 11 month old. The gene expression profiles were compared, and selected genes that showed either increased or decreased expression by a cut-off of 1.5 folds, p< 0.05. The results showed that many genes that are involved in lipid metabolism were upregulated in Smurf1-/- livers. These results also indicate that Smurf1 plays a more prominent role in the liver than Smurf2.
2018-12-19 | GSE113995 | GEO
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