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Lens epithelial cell transcriptome reprogramming at 24 hours post cataract surgery (PCS) in wild type (WT) and β8 integrin Conditional Knockout (β8ITGcKO) mice.

ABSTRACT: This trancriptome analysis reveals the first detailed analysis on how the remnant lens epithelial cells (LECs) greatly reprogram their transcriptome by 24 hours post cataract surgery (PCS) and the dependence of this phenomenom on endogenous β8 integrin gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE145492 | GEO | 2021/12/15

REPOSITORIES: GEO

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Lens epithelial cell transcriptome reprogramming at 24 hours post cataract surgery

Project description:This trancriptome analysis reveals the first detailed analysis on how the remnant lens epithelial cells (LECs) greatly reprogram their transcriptome towards inflammation/fibrosis by 24 hours post cataract surgery (PCS).

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Lens epithelial cell transcriptome reprogramming at 48 hours post cataract surgery (PCS) in wild type (WT) and Fibronectin Conditional Knockout (FNcKO) mice

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Expression data from lens epithelial cells (LECs) from Shumiya cataract rats (SCR) with or without cataract (Cat+ or Cat-)

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The influence of sex and age on the lens injury response

Project description:The purpose of this study was to investigate/characterize age- and sex-dependent changes in transcriptomic profile in a mouse model of cataract surgery that mimics human cataract surgery. This surgery involves the removal of lens fiber cells (LFC) leaving behind the lens capsule and associated lens epithelial cells (LEC). The lens capsule and associated remnant LECs were harvested either following cataract surgery (0 hour) or 24 hours later. Fiber cells were collected at the time of surgery, equivalent to 0 hour, and analyzed separately from epithelial cells. For samples from LEC, each biological replicate is a pool of 5 lens capsules from 5 independent mice. For samples from LFC, each biological replicate is a pool of 2 fiber cell masses from two independent mice. Mice were either 24 months old (Aged), or 3 months old (Young).

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Lens epithelial cell transcriptome reprogramming at 24 hours post cataract surgery (PCS) in wild type (WT) and β8 integrin Conditional Knockout (β8ITGcKO) mice.

Project description:Lens epithelial cell transcriptome reprogramming at 24 hours post cataract surgery (PCS) in wild type (WT) and β8 integrin Conditional Knockout (β8ITGcKO) mice.

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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.

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Expression data from lens epithelial cells (LECs) from Shumiya cataract rats (SCR) with or without cataract (Cat+ or Cat-)

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Lens epithelial cell transcriptome reprogramming at 48 hours post cataract surgery (PCS) in wild type (WT) and Fibronectin Conditional Knockout (FNcKO) mice

Project description:Lens epithelial cell transcriptome reprogramming at 48 hours post cataract surgery (PCS) in wild type (WT) and Fibronectin Conditional Knockout (FNcKO) mice

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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.

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