Expression and function of PDGF-α in columnar epithelial cells of age-related cataracts patients

Wei, Jinrong; Tang, Huaqiao; Xu, Zequan; Li, Bin; Xie, Liwei; Guo-li, XU

doi:10.4238/2015.october.26.28

Cited by 6 publications

(5 citation statements)

References 19 publications

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“…The observed single fold increase in AG would correspondingly increase the AGE-related crystallins (glycated forms) [21] and a 5-fold accumulation of sorbitol due to glucose conversion in MG induced cells have been observed (Figure 3). The aggregation of modified crystallins is known to be important for cataract formation [22] and the gravity of the cataract formation is emulated in the form of improved expression of PDGF [23]. The inflammation of the damaged lens tissues and the increased opacity of the lens coincides with the increase in the expression of PDGF explains the pathogenicity of cataract [23,24].…”

Section: Discussionmentioning

confidence: 99%

“…The aggregation of modified crystallins is known to be important for cataract formation [22] and the gravity of the cataract formation is emulated in the form of improved expression of PDGF [23]. The inflammation of the damaged lens tissues and the increased opacity of the lens coincides with the increase in the expression of PDGF explains the pathogenicity of cataract [23,24]. GG, known to be an inhibitor of AR in the cataract tissues effectively reduced the accumulation of sorbitol [1] when treated and could reverse the effect of cataract (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

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Protective Effect of β-Glucogallin on Damaged Cataract Against Methylglyoxal Induced Oxidative Stress in Cultured Lens Epithelial Cells

Liu

2019

Med Sci Monit

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Backgroundβ-glucogallin (GG) is one of the major plant polyphenolic antioxidants that have been associated with positive effects on human health and are crucial in the developing defense mechanism against the risk of diseases. However, reports on the protective mechanism of GG in lens epithelial cells are limited.Material/MethodsARPE-19 cells (a human retinal epithelial cell line) were exposed to methylglyoxal (MG) with or without GG to illuminate the protective role of GG in counteracting the cataract signaling.ResultsCells predisposed to MG demonstrated an increase in oxidative stress with augmented (P<0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes. In addition, the expression of aldose reductase (AR) was increased to 2-fold with accumulated sorbitol in MG exposed cells compared to control. On the other hand, cells exposed to MG evidenced a 3-fold increase in RAGE (receptor for advanced glycation end products) and a 2-fold increase in NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) expression compared to control cells. Intriguingly, lens epithelial cells pre-treated with GG attenuated the reactive oxygen species levels with improved antioxidant enzymes. Simultaneously, the levels of AR and other inflammatory cytokines were observed in the levels closer to control cells in GG pre-treated cells.ConclusionsThus, the results of the present investigation show that GG may be a potential drug for the prevention of cataract development and progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective Effect of β-Glucogallin on Damaged Cataract Against Methylglyoxal Induced Oxidative Stress in Cultured Lens Epithelial Cells

Liu

2019

Med Sci Monit

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“…In addition, advanced glycation endproducts could enhance the TGF-beta2-mediated EMT during PCO and might participate in aging and diabetes-related fibrosis 11 . Although EMT was an obvious event in age-related cataract tissues 27 , the pathological role of EMT remains unknown in the formation process of diabetic cataract. As vimentin and alpha-SMA are commonly chosen as EMT markers 28–31 , over-productions of vimentin and alpha-SMA in diabetic cataract LECs were found in our study, suggesting that LECs were undergoing EMT in diabetic cataract development.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1

Zhang

Wang

et al. 2017

Sci Rep

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Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process in development, fibrosis, and metastasis. During the process, epithelial cells lose their morphology and transcriptional program, and transdifferentiate to mesenchymal cells. It has been reported that lens epithelial cells undergo EMT during cataract formation, and regulation of microRNAs on genes is associated with lens development. However, the molecular mechanisms of this regulation in diabetic cataract still need to be investigated. In the present study, the expression of E-cadherin was downregulated, while the expression of alpha-SMA and vimentin was upregulated in diabetic cataract tissues and the in vitro model, suggesting the involvement of EMT in diabetic cataract formation. Results of miRNA profiling demonstrated that miR-30a was markedly downregulated in diabetic cataract tissues. Overexpression of miR-30a-5p decreased SNAI1, a known modulator of EMT, and the expression of vimentin and alpha-SMA in our diabetic cataract model in vitro. It is concluded that EMT is involved in human diabetic cataract, and upregulation of miR-30a can repress EMT through its targeting of SNAI1 in lens epithelial cells, which make miR-30a a novel target of therapeutic intervention for human diabetic cataract.

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“…SP1 specific protein, HG high glucose, LECs lens epithelial cells. *P < 0.05 in diabetes-related fibrosis and diabetic cataract development (Zhang et al 2017a;Taiyab et al 2016;Wei et al 2015). Via the prediction of microRNA.org, and TargetScan, SP1 is highly conserved to be the target of miR-199a.…”

Section: Discussionmentioning

confidence: 99%

microRNA-199a-5p regulates epithelial-to-mesenchymal transition in diabetic cataract by targeting SP1 gene

Liu

Gong

Yang

et al. 2020

Mol Med

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Background As a common ocular complication of diabetes mellitus, diabetic cataract is becoming a leading cause of visual impairment. The progression of diabetic cataract progression involves epithelial-to-mesenchymal transition (EMT), the precise role of which remains to be investigated. As microRNAs (miRNAs) are suggested to be involved in the pathogenesis of many diseases, identification of aberrantly expressed miRNAs in diabetic lens epithelial cells (LECs) and their targets may provide insights into our understanding of diabetic cataract and potential therapeutic targets. Methods Diabetic cataract capsules and LECs exposed to high glucose (25 mmol/L, 1–5 days) were used to mimic the model. Quantitative RT-PCR was performed to evaluate the differential expression of miRNA. Dual luciferase reporter assay was used to identify the binding target of miR-199a-5p. The expression of EMT-associated proteins was determined by immunofluorescence and Western blot analysis. Results Our results showed the differential expression of miR-9, -16, -22, -199a and -204. MiR-199a was downregulated in diabetic cataract capsule and hyperglycemia-conditioned human LECs. Specific protein 1 could be directly targeted and regulated by miR-199a in LECs and inhibit EMT in diabetic LECs. Conclusion Our findings implied miR-199a could be a therapeutic target by regulating SP1 directly to affect EMT in diabetic cataract and provided novel insights into the pathogenesis of diabetic cataract.

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Expression and function of PDGF-α in columnar epithelial cells of age-related cataracts patients

Abstract: ABSTRACT. We studied the expression and function of plateletderived growth factor A (PDGF-α) in the lens epithelial cells of cataracts patients. Ninety age-related cataracts patients were recruited in our hospital

Cited by 6 publications

References 19 publications

Protective Effect of β-Glucogallin on Damaged Cataract Against Methylglyoxal Induced Oxidative Stress in Cultured Lens Epithelial Cells

Protective Effect of β-Glucogallin on Damaged Cataract Against Methylglyoxal Induced Oxidative Stress in Cultured Lens Epithelial Cells

MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1

microRNA-199a-5p regulates epithelial-to-mesenchymal transition in diabetic cataract by targeting SP1 gene

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