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      MiR-195 inhibits the ubiquitination and degradation of YY1 by Smurf2, and induces EMT and cell permeability of retinal pigment epithelial cells

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          Abstract

          The dysregulated microRNAs (miRNAs) are involved in diabetic retinopathy progression. Epithelial mesenchymal transition (EMT) and cell permeability are important events in diabetic retinopathy. However, the function and mechanism of miR-195 in EMT and cell permeability in diabetic retinopathy remain largely unclear. Diabetic retinopathy models were established using streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-stimulated ARPE-19 cells. Retina injury was investigated by hematoxylin–eosin (HE) staining. EMT and cell permeability were analyzed by western blotting, immunofluorescence, wound healing, and FITC-dextran assays. MiR-195 expression was detected via qRT-PCR. YY1, VEGFA, Snail1, and Smurf2 levels were detected via western blotting. The interaction relationship was analyzed via ChIP, Co-IP, or dual-luciferase reporter assay. The retina injury, EMT, and cell permeability were induced in STZ-induced diabetic mice. HG induced EMT and cell permeability in ARPE-19 cells. MiR-195, YY1, VEGFA, and Snail1 levels were enhanced, but Smurf2 abundance was reduced in STZ-induced diabetic mice and HG-stimulated ARPE-19 cells. VEGFA knockdown decreased Snail1 expression and attenuated HG-induced EMT and cell permeability. YY1 silence reduced VEGFA and Snail1 expression, and mitigated HG-induced EMT and cell permeability. YY1 could bind with VEGFA and Snail1, and it was degraded via Smurf2-mediated ubiquitination. MiR-195 knockdown upregulated Smurf2 to decrease YY1 expression and inhibited HG-induced EMT and cell permeability. MiR-195 targeted Smurf2, increased expression of YY1, VEGFA, and Snail1, and promoted HG-induced EMT and cell permeability. MiR-195 promotes EMT and cell permeability of HG-stimulated ARPE-19 cells by increasing VEGFA/Snail1 via inhibiting the Smurf2-mediated ubiquitination of YY1.

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          Diabetic retinopathy.

          Tien Wong, Chui Ming Gemmy Cheung, Michael Larsen … (2016)
          Diabetic retinopathy (DR) is a common complication of diabetes mellitus and is a major cause of vision loss in middle-aged and elderly people. One-third of people with diabetes have DR. Severe stages of DR include proliferative DR, caused by the abnormal growth of new retinal blood vessels, and diabetic macular oedema, in which there is exudation and oedema in the central part of the retina. DR is strongly associated with a prolonged duration of diabetes, hyperglycaemia and hypertension. It is traditionally regarded as a microvascular disease, but retinal neurodegeneration is also involved. Complex interrelated pathophysiological mechanisms triggered by hyperglycaemia underlie the development of DR. These mechanisms include genetic and epigenetic factors, increased production of free radicals, advanced glycosylation end products, inflammatory factors and vascular endothelial growth factor (VEGF). Optimal control of blood glucose and blood pressure in individuals with diabetes remains the cornerstone for preventing the development and arresting the progression of DR. Anti-VEGF therapy is currently indicated for diabetic macular oedema associated with vision loss, whereas laser photocoagulation prevents severe vision loss in eyes with proliferative DR. These measures, together with increasing public awareness and access to regular screening for DR with retinal photography, and the development of new treatments to address early disease stages, will lead to better outcomes and prevent blindness for patients with DR.
          Article 0 comments Cited 285 times – based on 0 reviews     Review now
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            Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications

            Silvia Juliana Serrano-Gomez, Mazvita Maziveyi, Suresh K Alahari (2016)
            The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
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              Diabetic retinopathy: hyperglycaemia, oxidative stress and beyond.

              Hans-Peter Hammes (2018)
              Diabetic retinopathy remains a relevant clinical problem. In parallel with diagnostic and therapeutic improvements, the role of glycaemia and reactive metabolites causing cell stress and biochemical abnormalities as treatment targets needs continuous re-evaluation. Furthermore, the basic mechanisms of physiological angiogenesis, remodelling and pruning give important clues about the origins of vasoregression during the very early stages of diabetic retinopathy and can be modelled in animals. This review summarises evidence supporting a role for the neurovascular unit-composed of neuronal, glial and vascular cells-as a responder to the biochemical changes imposed by reactive metabolites and high glucose. Normoglycaemic animal models developing retinal degeneration, provide valuable information about common pathways downstream of progressive neuronal damage that induce vasoregression, as in diabetic models. These models can serve to assess novel treatments addressing the entire neurovascular unit for the benefit of early diabetic retinopathy.
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                Author and article information

                Contributors
                Fei Liu:
                ORCID: http://orcid.org/0000-0002-7601-2556
                feiiuyh887@163.com
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 15 July 2021
                Publication date PMC-release: 15 July 2021
                Publication date Collection: July 2021
                Volume: 12
                Issue: 7
                Electronic Location Identifier: 708
                Affiliations
                GRID grid.412455.3, Department of Ophthalmology, , The Second Affiliated Hospital of Nanchang University, ; Nanchang, 330006 Jiangxi Province P. R. China
                Author information
                http://orcid.org/0000-0002-7601-2556
                Article
                Publisher ID: 3956
                DOI: 10.1038/s41419-021-03956-6
                PMC ID: 8282777
                PubMed ID: 34267179
                SO-VID: a3970e12-81a1-4ab5-af91-2f7940c4dbbb
                Copyright © © The Author(s) 2021
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 19 February 2021
                Date accepted : 10 June 2021
                Funding
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
                Funded by: This work was supported by the National Natural Science Foundation of China (NO. 81660164 & NO.81860176), the Natural Science Foundation Key Program of Jiangxi Province (NO. 20171ACB20036), the Scientific Research Program of Jiangxi Health and Family Planning Commission (NO. 2017A238) and the Doctor Start-up Fund of the Second Affiliated Hospital of Nanchang University (NO. B1728#).
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                Subject: Article
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                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Cell biology
                Keywords: mechanisms of disease,diabetes
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: mechanisms of disease, diabetes

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