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MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1

BACKGROUND: Pancreatic β-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic β-cell dysfunction. However, the detailed mechanisms remain largely unknown. METHODS: RT-qPCR, western blotting...

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Autores principales: Lv, Lixia, Wang, Xiumin, Shen, Jinhua, Cao, Ying, Zhang, Qin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9284709/
https://www.ncbi.nlm.nih.gov/pubmed/35841066
http://dx.doi.org/10.1186/s13098-022-00869-y
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author Lv, Lixia
Wang, Xiumin
Shen, Jinhua
Cao, Ying
Zhang, Qin
author_facet Lv, Lixia
Wang, Xiumin
Shen, Jinhua
Cao, Ying
Zhang, Qin
author_sort Lv, Lixia
collection PubMed
description BACKGROUND: Pancreatic β-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic β-cell dysfunction. However, the detailed mechanisms remain largely unknown. METHODS: RT-qPCR, western blotting, and immunofluorescence assays were used to evaluate PRMT1 and miR-574-3p levels. Cell Counting Kit-8, Advanced Dlycation End products (AGEs), Reactive Oxygen Species (ROS), and glucose-stimulated insulin secretion were assayed, and flow cytometry and RT-qPCR were performed to detect the role of PRMT1 and miR-574-3p in MIN6 cells. Luciferase reporter assays were performed to determine the interactions between PRMT1 and miR-574-3p. RESULTS: High-glucose treatment resulted in the high expression of PRMT1. PRMT1 silencing could alleviate the reduced proliferation, insulin secretion, and GLUT1 level, in addition to suppressing the induced apoptosis, and AGEs and ROS levels, under high glucose conditions. MiR-574-3p was established as an upstream regulator of PRMT1 using luciferase reporter assays. More importantly, miR-574-3p reversed the effect of PRMT1 silencing in MIN6 cells. CONCLUSIONS: miR-574-3p suppresses glucose toxicity-induced pancreatic β-cell dysfunction by targeting PRMT1. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13098-022-00869-y.
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spelling pubmed-92847092022-07-16 MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1 Lv, Lixia Wang, Xiumin Shen, Jinhua Cao, Ying Zhang, Qin Diabetol Metab Syndr Research BACKGROUND: Pancreatic β-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic β-cell dysfunction. However, the detailed mechanisms remain largely unknown. METHODS: RT-qPCR, western blotting, and immunofluorescence assays were used to evaluate PRMT1 and miR-574-3p levels. Cell Counting Kit-8, Advanced Dlycation End products (AGEs), Reactive Oxygen Species (ROS), and glucose-stimulated insulin secretion were assayed, and flow cytometry and RT-qPCR were performed to detect the role of PRMT1 and miR-574-3p in MIN6 cells. Luciferase reporter assays were performed to determine the interactions between PRMT1 and miR-574-3p. RESULTS: High-glucose treatment resulted in the high expression of PRMT1. PRMT1 silencing could alleviate the reduced proliferation, insulin secretion, and GLUT1 level, in addition to suppressing the induced apoptosis, and AGEs and ROS levels, under high glucose conditions. MiR-574-3p was established as an upstream regulator of PRMT1 using luciferase reporter assays. More importantly, miR-574-3p reversed the effect of PRMT1 silencing in MIN6 cells. CONCLUSIONS: miR-574-3p suppresses glucose toxicity-induced pancreatic β-cell dysfunction by targeting PRMT1. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13098-022-00869-y. BioMed Central 2022-07-15 /pmc/articles/PMC9284709/ /pubmed/35841066 http://dx.doi.org/10.1186/s13098-022-00869-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Lv, Lixia
Wang, Xiumin
Shen, Jinhua
Cao, Ying
Zhang, Qin
MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
title MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
title_full MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
title_fullStr MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
title_full_unstemmed MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
title_short MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
title_sort mir-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing prmt1
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9284709/
https://www.ncbi.nlm.nih.gov/pubmed/35841066
http://dx.doi.org/10.1186/s13098-022-00869-y
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