دورية أكاديمية
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SUMOylation of GMFB regulates its stability and function in retinal pigment epithelial cells under hyperglycemia.

التفاصيل البيبلوغرافية
العنوان: SUMOylation of GMFB regulates its stability and function in retinal pigment epithelial cells under hyperglycemia.
المؤلفون: Sun W; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Wang J; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Medical Genetics, School of Medicine, Tongji University, Shanghai 200065, China., Liu C; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Gao F; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Ou Q; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Pharmacology, School of Medicine, Tongji University, Shanghai 200065, China., Tian H; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Xu J; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Zhang J; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Pharmacology, School of Medicine, Tongji University, Shanghai 200065, China., Li J; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Xu J; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Jia S; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China., Zhang J; Department of Ophthalmology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai 200025, China., Xu G; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Pharmacology, School of Medicine, Tongji University, Shanghai 200065, China. Electronic address: gtxu@tongji.edu.cn., Huang J; Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. Electronic address: jyhuanj@shsmu.edu.cn., Jin C; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China. Electronic address: 12060@tongji.edu.cn., Lu L; Department of Ophthalmology of Shanghai Tongji Hospital and Laboratory of Clinical Visual Science of Tongji Eye Institute, Tongji University, Shanghai 200065, China; Department of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200065, China. Electronic address: lulixia@tongji.edu.cn.
المصدر: International journal of biological macromolecules [Int J Biol Macromol] 2024 May; Vol. 268 (Pt 2), pp. 131678. Date of Electronic Publication: 2024 Apr 22.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 7909578 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0003 (Electronic) Linking ISSN: 01418130 NLM ISO Abbreviation: Int J Biol Macromol Subsets: MEDLINE
أسماء مطبوعة: Publication: Amsterdam : Elsevier
Original Publication: Guildford, Eng., IPC Science and Technology Press.
مواضيع طبية MeSH: Hyperglycemia*/metabolism , Protein Stability* , Retinal Pigment Epithelium*/metabolism , Signal Transduction* , Sumoylation*, Humans ; Cell Line ; Diabetic Retinopathy/metabolism ; Diabetic Retinopathy/pathology ; Epithelial Cells/metabolism ; NF-kappa B/metabolism ; SUMO-1 Protein/metabolism ; Glia Maturation Factor
مستخلص: Background: Glia maturation factor beta (GMFB) is a growth and differentiation factor that acts as an intracellular regulator of signal transduction pathways. The small ubiquitin-related modifier (SUMO) modification, SUMOylation, is a posttranslational modification (PTM) that plays a key role in protein subcellular localization, stability, transcription, and enzymatic activity. Recent studies have highlighted the importance of SUMOylation in the inflammation and progression of numerous diseases. However, the relationship between GMFB and SUMOylation is unclear.
Results: Here, we report for the first time that GMFB and SUMO1 are markedly increased in retinal pigment epithelial (RPE) cells at the early stage of diabetes mellitus (DM) under hyperglycemia. The GMFΒ protein could be mono-SUMOylated by SUMO1 at the K20, K35, K58 or K97 sites. SUMOylation of GMFB led to its increased protein stability and subcellular translocation. Furthermore, deSUMOylation of GMFΒ downregulates multiple signaling pathways, including the Jak-STAT signaling pathway, p38 pathway and NF-kappa B signaling pathway.
Conclusions: This work provides novel insight into the role of SUMOylated GMFB in RPE cells and provides a novel therapeutic target for diabetic retinopathy (DR).
Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest.
(Copyright © 2024. Published by Elsevier B.V.)
فهرسة مساهمة: Keywords: Glia maturation factor-β (GMFB); Hyperglycemia; Protein stability; Retinal pigment epithelial cells; SUMOylation
المشرفين على المادة: 0 (NF-kappa B)
0 (SUMO-1 Protein)
0 (Glia Maturation Factor)
تواريخ الأحداث: Date Created: 20240424 Date Completed: 20240524 Latest Revision: 20240610
رمز التحديث: 20240611
DOI: 10.1016/j.ijbiomac.2024.131678
PMID: 38657921
قاعدة البيانات: MEDLINE
الوصف
تدمد:1879-0003
DOI:10.1016/j.ijbiomac.2024.131678