ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021
LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Long Non-Coding RNAs and Proliferative Retinal Diseases.Pharmaceutics · 2023Review
- Noncoding RNAs Are Promising Therapeutic Targets for Diabetic Retinopathy: An Updated Review (2017-2022).Biomolecules · 2022Review
- Diabetic Retinopathy: Are lncRNAs New Molecular Players and Targets?Antioxidants (Basel, Switzerland) · 2022Review
- Impact of Long Noncoding RNA LINC00673 Genetic Variants on Susceptibility to Diabetic Retinopathy.Frontiers in genetics · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLong noncoding RNA (LncRNA) LINC00673 has been proven to play critical roles in cancer biology, while its role in other diseases is unknown. It has been reported that LINC00673 could interact with p53, a critical player in diabetes and diabetic complications, suggesting that LINC00673 may also participate in diabetic retinopathy (DR). This study aimed to investigate the role of LINC00673 in DR.
methodsThe present study included 3 groups of participants, including DR group, diabetes (DB) group, and healthy control (Control) group. Flow cytometry was utilized to determine cell apoptosis. Proteins and messenger RNAs (mRNAs) were estimated by Western blot and quantitative reverse transcription PCR (qRT-PCR), respectively.
resultsLINC00673 was downregulated in plasma samples of DR patients (n=60) in comparison with the healthy controls (n=60) and negatively correlated with p53 only across DR patients but not across the healthy controls. In retinal pigment epithelial cells (RPECs), high glucose treatment downregulated LINC00673. Moreover, LINC00673 overexpression downregulated p53 and decreased RPEC apoptosis, while LINC00673 silencing upregulated p53 and increased RPEC apoptosis. In addition, p53 overexpression reduced the effects of LINC00673 overexpression.
conclusionLINC00673 is downregulated in DR patients and regulates RPEC apoptosis via negatively regulating p53.
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