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LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53

BACKGROUND: Long 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 ma...

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Autores principales: Cheng, Yan, Zhu, Yanxia, Ma, Linli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8520846/
https://www.ncbi.nlm.nih.gov/pubmed/34675574
http://dx.doi.org/10.2147/DMSO.S298185
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author Cheng, Yan
Zhu, Yanxia
Ma, Linli
author_facet Cheng, Yan
Zhu, Yanxia
Ma, Linli
author_sort Cheng, Yan
collection PubMed
description BACKGROUND: Long 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. METHODS: The 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. RESULTS: LINC00673 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. CONCLUSION: LINC00673 is downregulated in DR patients and regulates RPEC apoptosis via negatively regulating p53.
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spelling pubmed-85208462021-10-20 LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53 Cheng, Yan Zhu, Yanxia Ma, Linli Diabetes Metab Syndr Obes Original Research BACKGROUND: Long 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. METHODS: The 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. RESULTS: LINC00673 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. CONCLUSION: LINC00673 is downregulated in DR patients and regulates RPEC apoptosis via negatively regulating p53. Dove 2021-10-13 /pmc/articles/PMC8520846/ /pubmed/34675574 http://dx.doi.org/10.2147/DMSO.S298185 Text en © 2021 Cheng et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Cheng, Yan
Zhu, Yanxia
Ma, Linli
LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53
title LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53
title_full LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53
title_fullStr LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53
title_full_unstemmed LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53
title_short LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53
title_sort lncrna linc00673 is downregulated in diabetic retinopathy and regulates the apoptosis of retinal pigment epithelial cells via negatively regulating p53
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8520846/
https://www.ncbi.nlm.nih.gov/pubmed/34675574
http://dx.doi.org/10.2147/DMSO.S298185
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