N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract

N6-methyladenosine (m6A) is the most prevalent eukaryotic messenger RNA modification. Diabetic cataract (DC) is caused by high glucose (HG) in diabetes mellitus. However, the regulatory mechanism of m6A in the DC pathogenesis is poorly understood. In present research, we performed the m6A-RNA immuno...

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Main Authors: Jun Yang, Jingshu Liu, Shaozhen Zhao, Fang Tian
Format: Article
Language:English
Published: Elsevier 2020-06-01
Series:Molecular Therapy: Nucleic Acids
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2162253120300743
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author Jun Yang
Jingshu Liu
Shaozhen Zhao
Fang Tian
author_facet Jun Yang
Jingshu Liu
Shaozhen Zhao
Fang Tian
author_sort Jun Yang
collection DOAJ
description N6-methyladenosine (m6A) is the most prevalent eukaryotic messenger RNA modification. Diabetic cataract (DC) is caused by high glucose (HG) in diabetes mellitus. However, the regulatory mechanism of m6A in the DC pathogenesis is poorly understood. In present research, we performed the m6A-RNA immunoprecipitation sequencing (MeRIP-Seq) analysis and detected the m6A modification profile in the HG- or normal glucose (NG)-induced human lens epithelial cells (HLECs). Results revealed that methyltransferase-like 3 (METTL3) was upregulated in the DC tissue specimens and HG-induced HLECs. Besides, total m6A modification level was higher in the HG-induced HLECs. Functionally, METTL3 knockdown promoted the proliferation and repressed the apoptosis of HLECs induced by HG. MeRIP-Seq analysis revealed that ICAM-1 might act as the target of METTL3. Mechanistically, METTL3 targets the 3′ UTR of ICAM-1 to stabilize mRNA stability. In conclusion, this research identified the regulation of METTL3 in the HG-induced HLECs, providing a potential insight of the m6A modification for DC.
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spelling doaj.art-f2ac90cbf04c4347a7e35375b1e92e492022-12-22T02:04:50ZengElsevierMolecular Therapy: Nucleic Acids2162-25312020-06-0120111116N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic CataractJun Yang0Jingshu Liu1Shaozhen Zhao2Fang Tian3Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, ChinaTianjin University of Traditional Chinese Medicine, Tianjin, ChinaEye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, China; Corresponding author: Shaozhen Zhao, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, China.Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, China; Corresponding author: Fang Tian, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, China.N6-methyladenosine (m6A) is the most prevalent eukaryotic messenger RNA modification. Diabetic cataract (DC) is caused by high glucose (HG) in diabetes mellitus. However, the regulatory mechanism of m6A in the DC pathogenesis is poorly understood. In present research, we performed the m6A-RNA immunoprecipitation sequencing (MeRIP-Seq) analysis and detected the m6A modification profile in the HG- or normal glucose (NG)-induced human lens epithelial cells (HLECs). Results revealed that methyltransferase-like 3 (METTL3) was upregulated in the DC tissue specimens and HG-induced HLECs. Besides, total m6A modification level was higher in the HG-induced HLECs. Functionally, METTL3 knockdown promoted the proliferation and repressed the apoptosis of HLECs induced by HG. MeRIP-Seq analysis revealed that ICAM-1 might act as the target of METTL3. Mechanistically, METTL3 targets the 3′ UTR of ICAM-1 to stabilize mRNA stability. In conclusion, this research identified the regulation of METTL3 in the HG-induced HLECs, providing a potential insight of the m6A modification for DC.http://www.sciencedirect.com/science/article/pii/S2162253120300743N6-methyladenosinehuman lens epithelial cellsdiabetic cataractMETTL3ICAM-1
spellingShingle Jun Yang
Jingshu Liu
Shaozhen Zhao
Fang Tian
N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract
Molecular Therapy: Nucleic Acids
N6-methyladenosine
human lens epithelial cells
diabetic cataract
METTL3
ICAM-1
title N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract
title_full N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract
title_fullStr N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract
title_full_unstemmed N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract
title_short N6-Methyladenosine METTL3 Modulates the Proliferation and Apoptosis of Lens Epithelial Cells in Diabetic Cataract
title_sort n6 methyladenosine mettl3 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract
topic N6-methyladenosine
human lens epithelial cells
diabetic cataract
METTL3
ICAM-1
url http://www.sciencedirect.com/science/article/pii/S2162253120300743
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