Quantitative analysis of injury-induced anterior subcapsular cataract in the mouse: a model of lens epithelial cells proliferation and epithelial-mesenchymal transition

Xiao, Wei; Chen, Xiaoyun; Li, Weihua; Ye, Shaobi; Wang, Wencong; Luo, Lixia; Liu, Yizhi

doi:10.1038/srep08362

Cited by 41 publications

(38 citation statements)

References 27 publications

(38 reference statements)

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“…37 Briefly, the injured mice were killed and their eyes were enucleated. And then the lens were isolated under a dissecting microscope and fixed in 100% methanol for 1 h at RT.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-26a and -26b inhibit lens fibrosis and cataract by negatively regulating Jagged-1/Notch signaling pathway

et al. 2017

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Fibrosis is a chronic process involving development and progression of multiple diseases in various organs and is responsible for almost half of all known deaths. Epithelial–mesenchymal transition (EMT) is the vital process in organ fibrosis. Lens is an elegant biological tool to investigate the fibrosis process because of its unique biological properties. Using gain- and loss-of-function assays, and different lens fibrosis models, here we demonstrated that microRNA (miR)-26a and miR-26b, members of the miR-26 family have key roles in EMT and fibrosis. They can significantly inhibit proliferation, migration, EMT of lens epithelial cells and lens fibrosis in vitro and in vivo. Interestingly, we revealed that the mechanisms of anti-EMT effects of miR-26a and -26b are via directly targeting Jagged-1 and suppressing Jagged-1/Notch signaling. Furthermore, we provided in vitro and in vivo evidence that Jagged-1/Notch signaling is activated in TGFβ2-stimulated EMT, and blockade of Notch signaling can reverse lens epithelial cells (LECs) EMT and lens fibrosis. Given the general involvement of EMT in most fibrotic diseases, cancer metastasis and recurrence, miR-26 family and Notch pathway may have therapeutic uses in treating fibrotic diseases and cancers.

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“…37 Briefly, the injured mice were killed and their eyes were enucleated. And then the lens were isolated under a dissecting microscope and fixed in 100% methanol for 1 h at RT.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-26a and -26b inhibit lens fibrosis and cataract by negatively regulating Jagged-1/Notch signaling pathway

et al. 2017

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“…LncRNA XLOC_009704/n344497, also known as lncRNA RMST, was down-regulated in nuclear ARC compared to transparent lens capsules. RMST is an emerging regulatory lncRNA in epithelial-to-mesenchymal transition (EMT) and cell differentiation [45,46], which may be related to the pathogenesis of cataract [47,48]. Previous studies identified a microRNA, miR-135a, whose expression was correlated to the lncRNA RMST.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA H19 Regulates Human Lens Epithelial Cells Function

Liu

Shan

et al. 2018

Cell Physiol Biochem

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Background/Aims: Age-related cataract (ARC) remains the leading cause of visual impairment among the elderly population. Long non-coding RNAs (lncRNAs) have emerged as potential regulators in many ocular diseases. However, the role of lncRNAs in nuclear ARC, a subtype of ARC, requires further elucidation. Methods: LncRNA sequencing was performed to identify differentially expressed lncRNAs between the capsules of transparent and nuclear ARC lenses. Expression validation was confirmed by qRT-PCR. MTT assay, Calcein-AM and propidium iodide double staining, Rhodamine 123 and Hoechst double staining, EdU and transwell assay were used to determine the role of H19 or miR-675 in the viability, apoptosis, proliferation and migration of primary cultured human lens epithelial cells (HLECs). Bioinformatics and luciferase reporter assays were used to identify the binding target of miR-675. Results: Sixty-three lncRNAs are differentially expressed between the capsules of transparent and nuclear ARC lenses. One top abundantly expressed lncRNA, H19, is significantly up-regulated in the nuclear ARC lens capsules and positively associated with nuclear ARC grade. H19 knockdown accelerates apoptosis development and reduces the proliferation and migration of HLECs upon oxidative stress. H19 is the precursor of miR-675, and a reduction of H19 inhibits miR-675 expression. miR-675 regulates CRYAA expression by targeting the binding site within the 3’UTR. Moreover, miR-675 increases the proliferation and migration while decreasing the apoptosis of HLECs upon oxidative stress. Conclusion: H19 regulates HLECs function through miR-675-mediated CRYAA expression. This finding would provide a novel insight into the pathogenesis of nuclear ARC.

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“…All animal experiments were approved by the Animal Ethics Committee of Kunming Medical University. The mouse model of injury‐induced ASC was established as described previously . Before the surgical procedure, the mice (body weight [BW] = 30‐50 g, n = 6, male) were given a single intraperitoneal injection of pentobarbital sodium (70 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

2',3'‐Cyclic‐nucleotide 3'‐phosphodiesterase contributes to epithelial‐mesenchymal transition of lens epithelial cells through the notch signalling pathway

Zhao

Wang

2019

Cell Proliferation

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Objectives Fibrosis is a complex process involved in multiple diseases that result in organ injury and failure. Cataract, one common form of ocular fibrosis, is a main cause of blindness worldwide, and surgery may be the only cure. In this regard, epithelial‐mesenchymal transition (EMT) of lens epithelial cells (LECs) is the primary cause of anterior subcapsular cataract (ASC). This study aimed to investigate the mechanism by which 2',3'‐cyclic‐nucleotide 3'‐phosphodiesterase (CNPase) regulates the function of EMT in LECs. Materials and Methods A mouse model of ASC was used to observe the expression of CNPase in the lens and correlate its expression changes with lens EMT. Furthermore, the effects of CNPase on cell migration and cell proliferation were evaluated by transwell migration, wound healing and EdU staining assays. Finally, Western blotting and immunofluorescence were used to assess the mechanical properties potentially involved in the regulation of EMT by CNPase. Results The expression of CNPase was upregulated in LECs during the EMT process in mice with ASC. Notably, CNPase significantly promoted the proliferation, migration and EMT of LECs in vitro. Interestingly, the EMT‐promoting mechanism of CNPase may be achieved by targeting the Notch signalling pathway. Conclusions Considering the involvement of EMT in ASC, both CNPase and the Notch signalling pathway may be therapeutic targets for the treatment of cataracts.

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Quantitative analysis of injury-induced anterior subcapsular cataract in the mouse: a model of lens epithelial cells proliferation and epithelial-mesenchymal transition

Cited by 41 publications

References 27 publications

MicroRNA-26a and -26b inhibit lens fibrosis and cataract by negatively regulating Jagged-1/Notch signaling pathway

MicroRNA-26a and -26b inhibit lens fibrosis and cataract by negatively regulating Jagged-1/Notch signaling pathway

Long Non-Coding RNA H19 Regulates Human Lens Epithelial Cells Function

2',3'‐Cyclic‐nucleotide 3'‐phosphodiesterase contributes to epithelial‐mesenchymal transition of lens epithelial cells through the notch signalling pathway

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