ArticleInternational urology and nephrology2020
Silencing CCNG1 protects MPC-5 cells from high glucose-induced proliferation-inhibition and apoptosis-promotion via MDM2/p53 signaling pathway.
Article in International urology and nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 13 citations in OpenAlex.
- Recurrent single-CpG methylation differences and incomplete segregation in familial type 1 diabetes.Frontiers in immunology · 2026Article
- Molecular docking and antitumor evaluation of liposomal nanoformulations containing citrinin.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Hspb1 and Lgals3 in spinal neurons are closely associated with autophagy following excitotoxicity based on machine learning algorithms.PloS one · 2024Article
- BMP-9 Improves the Osteogenic Differentiation Ability over BMP-2 through p53 Signaling In Vitro in Human Periosteum-Derived Cells.International journal of molecular sciences · 2023Article
- Abnormal expression of miRNA-122 in cerebral infarction and related mechanism of regulating vascular endothelial cell proliferation and apoptosis by targeting CCNG1.Clinics (Sao Paulo, Brazil) · 2023Article
- Network pharmacology and molecular docking technology-based predictive study of the active ingredients and potential targets of rhubarb for the treatment of diabetic nephropathy.BMC complementary medicine and therapies · 2022Article
- Differential expression of cyclins CCNB1 and CCNG1 is involved in the chondrocyte damage of kashin-beck disease.Frontiers in genetics · 2022Article
- Transcriptome Analysis Reveal Candidate Genes and Pathways Responses to Lactate Dehydrogenase Inhibition (Oxamate) in Hyperglycemic Human Renal Proximal Epithelial Tubular Cells.Frontiers in endocrinology · 2022Article
- lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis.Journal of healthcare engineering · 2022Article
- Forsythoside A Alleviates High Glucose-Induced Oxidative Stress and Inflammation in Podocytes by Inactivating MAPK Signaling via MMP12 Inhibition.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
purposeDiabetic nephropathy (DN) is one of the most serious complications of diabetes mellitus and one of the most important causes of end-stage renal disease, but its pathogenesis has not been elucidated so far, and there is no effective treatment.
methodsDN models of rats and MPC-5 cells were established with streptozotocin (STZ) and high glucose (HG) in vivo and in vitro, respectively. Cell markers desmin and nephrin in foot kidney tissue were detected by Western blot. CCNG1 level in vitro was analyzed by Western blot and immunohistochemistry. CCK-8 assay and flow cytometry were conducted to analyze the effect of CCNG1 on HG-treated MPC-5 cells. Apoptosis-related proteins (Bcl-2, Bax and p53), CCNG1, and MDM2 were determined by RT-qPCR and Western blot.
resultsThe level of nephrin was decreased, while desmin was increased in STZ-induced DN rats and CCNG1 level was also enhanced by STZ. In vitro experiments indicated that MPC-5 cell viability was inhibited and apoptosis was induced by HG and we also found that CCNG1 expression was up-regulated by HG and negatively correlated with MDM2 level. The effects of HG on MPC-5 cell viability, apoptosis, and cell cycle were reversed by silencing CCNG1, but further deteriorated by overexpression of CCNG1. Furthermore, overexpression of MDM2 inhibited HG-induced MPC-5 cell injury and CCNG1 expression.
conclusionsThese findings revealed that down-regulation of CCNG1 has protection effects in DN that is mechanistically linked to MDM2-p53 pathways.
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