ArticleJournal of diabetes research2013
Impact of high glucose and proteasome inhibitor MG132 on histone H2A and H2B ubiquitination in rat glomerular mesangial cells.
Article in Journal of diabetes research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Unraveling the complexity of the histone code: implications for gene regulation and disease.Genome biology · 2026Review
- Morphological and structural alterations in skeletal muscle of STZ-induced diabetic rats revealed by light and electron microscopy.Journal of advanced veterinary and animal research · 2026Article
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
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- Development of necroptosis-related gene signature to predict the prognosis of colon adenocarcinoma.Frontiers in genetics · 2022Article
- Review
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- Butyrate ameliorates alcoholic fatty liver disease via reducing endotoxemia and inhibiting liver gasdermin D-mediated pyroptosis.Annals of translational medicine · 2021Article
- Increased co-expression of PSMA2 and GLP-1 receptor in cervical cancer models in type 2 diabetes attenuated by Exendin-4: A translational case-control study.EBioMedicine · 2021Article
- Apelin inhibited epithelial-mesenchymal transition of podocytes in diabetic mice through downregulating immunoproteasome subunits β5i.Cell death & disease · 2018Article
- Non-genetic mechanisms of diabetic nephropathy.Frontiers of medicine · 2017Review
- Maresin 1 Mitigates High Glucose-Induced Mouse Glomerular Mesangial Cell Injury by Inhibiting Inflammation and Fibrosis.Mediators of inflammation · 2017Article
- Genome-wide DNA methylation analysis identifies a metabolic memory profile in patient-derived diabetic foot ulcer fibroblasts.Epigenetics · 2014Article
- Posttranslational modification of mitochondrial transcription factor A in impaired mitochondria biogenesis: implications in diabetic retinopathy and metabolic memory phenomenon.Experimental eye research · 2014Article
- The role of ubiquitination and sumoylation in diabetic nephropathy.BioMed research international · 2014Review
- High glucose induces sumoylation of Smad4 via SUMO2/3 in mesangial cells.BioMed research international · 2014Article
- MG132 ameliorates kidney lesions by inhibiting the degradation of Smad7 in streptozotocin-induced diabetic nephropathy.Journal of diabetes research · 2014Article
- The genetics of diabetic nephropathy.Genes · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperglycemia plays a pivotal role in the development of diabetic nephropathy (DN) and may be related to epigenetic metabolic memory. One of the most crucial epigenetic mechanisms is histone modification, which is associated with the expression of a fibrosis factor in vascular injury. Aim .In this study, we investigated the ubiquitination of histones H2A and H2B to explore the epigenetic mechanisms of DN. MATERIALS AND
methodsThe GMCs were cultured as follows: normal group, high glucose group, mannitol group, and intervention group. After 12 hr, 24 hr, and 48 hr, histones ubiquitination, transforming growth factor-β (TGF-β), and fibronectin (FN) were measured using WB, RT-PCR, and IF.
resultHigh glucose can induce the upregulation of FN. H2A ubiquitination in GMCs increased in high glucose group (P < 0.01), whereas it decreased significantly in intervention group (P < 0.05). In contrast, H2B ubiquitination decreased with an increasing concentration of glucose, but it was recovered in the intervention group (P < 0.05). Expression of TGF-β changed in response to abnormal histone ubiquitination.
conclusionsThe high glucose may induce H2A ubiquitination and reduce H2B ubiquitination in GMCs. The changes of histone ubiquitination may be due in part to DN by activating TGF-β signaling pathway.
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