ArticleBMC endocrine disorders2021
LncRNA HCP5 knockdown inhibits high glucose-induced excessive proliferation, fibrosis and inflammation of human glomerular mesangial cells by regulating the miR-93-5p/HMGA2 axis.
Article in BMC endocrine disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- MicroRNA Changes Up to 24 h following Induced Hypoglycemia in Type 2 Diabetes.International journal of molecular sciences · 2022Trial
- Overexpression of LINC00472 alleviates diabetic kidney disease progression via the miR-21-5p/STAT3 axis.Renal failure · 2026Article
- Dysregulation of miR-302a-3p in diabetic nephropathy and its role in inflammatory response.BMC endocrine disorders · 2025Article
- MicroRNA let-7a mitigates the progression of oral submucous fibrosis by targeting high-mobility group AT-hook 2.Journal of dental sciences · 2025Article
- mTOR pathway: A key player in diabetic nephropathy progression and therapeutic targets.Genes & diseases · 2025Review
- Research progress on non-coding RNA regulatory networks and targeted therapy in diabetic nephropathy.Frontiers in endocrinology · 2025Review
- Multi-Omics Analysis Revealed the rSNPs Potentially Involved in T2DM Pathogenic Mechanism and Metformin Response.International journal of molecular sciences · 2024Article
- Exosomal lncRNA HCP5 derived from human bone marrow mesenchymal stem cells improves chronic periodontitis by miR-24-3p/Heliyon · 2024Article
- Roles of long noncoding RNAs in human inflammatory diseases.Cell death discovery · 2024Review
- LncRNA HCP5 is Highly Expressed in Gestational Diabetes Mellitus to Suppress Insulin Secretion.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- LncRNA HCP5 acts as a potential diagnostic biomarker and attenuates the inflammatory response in neonatal sepsis by targeting miR-138-5p/SIRT1.Central-European journal of immunology · 2024Article
- lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis.Journal of healthcare engineering · 2022Article
- Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2022Review
- Detection of SARS-CoV-2 infection by microRNA profiling of the upper respiratory tract.PloS one · 2022Article
- LncRNA KCNQ1OT1 promotes the development of diabetic nephropathy by regulating miR-93-5p/ROCK2 axis.Diabetology & metabolic syndrome · 2021Article
- Emerging Role of LncRNA Regulation for NLRP3 Inflammasome in Diabetes Complications.Frontiers in cell and developmental biology · 2021Review
- Identification of Hub Genes and Potential ceRNA Networks of Diabetic Nephropathy by Weighted Gene Co-Expression Network Analysis.Frontiers in genetics · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong non-coding RNAs (lncRNAs) are widely reported to be involved in the development of human diseases. HLA complex P5 (HCP5) deregulation is associated with various diseases. However, the function of HCP5 in diabetic nephropathy (DN) is unclear.
methodsHuman glomerular mesangial cells (HGMCs) were treated with high glucose (HG) to establish DN cell models. The expression of HCP5, miR-93-5p and high mobility group AT-hook 2 (HMGA2) mRNA was detected using quantitative polymerase chain reaction (QPCR). Cell proliferation and cell apoptosis were assessed using cell counting kit-8 (CCK-8) assay and flow cytometry assay, respectively. The expression of apoptosis- and fibrosis-related proteins and HMGA2 protein was quantified by western blot. The release of pro-inflammatory factor was checked using enzyme-linked immunosorbent assay (ELISA). The predicted relationship between miR-93-5p and HCP5 or HMGA2 was verified using dual-luciferase reporter assay, pull-down assay or RNA immunoprecipitation (RIP) assay.
resultsThe expression of HCP5 and HMGA2 was enhanced, while the expression of miR-93-5p was declined in DN serum samples and HG-treated HGMCs. HCP5 knockdown or miR-93-5p restoration ameliorated HG-induced HGMC proliferation, fibrosis and inflammation. MiR-93-5p was a target of HCP5, and miR-93-5p inhibition reversed the effects caused by HCP5 knockdown. Moreover, HMGA2 was a target of miR-93-5p, and HMGA2 overexpression abolished the effects of miR-93-5p restoration. HCP5 knockdown inhibited the AKT/mTOR signaling pathway.
conclusionHCP5 was implicated in DN progression by modulating the miR-93-5p/HMGA2 axis, which provided new insights into the understanding of DN pathogenesis.
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