ArticleInternational journal of clinical and experimental pathology2019
miR-216a-5p promotes mesangial cell proliferation by targeting FoxO1 in diabetic nephropathy.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- MiR-216a-5p protects against high glucose-induced HMC injury by targeting the HMGB1/RAGE signaling pathway.Frontiers in endocrinology · 2025Article
- Transfer of MicroRNA-216a-5p From Exosomes Secreted by Human Urine-Derived Stem Cells Reduces Renal Ischemia/Reperfusion Injury.Frontiers in cell and developmental biology · 2020Article
- Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic nephropathy (DN) is a leading cause of end-stage renal disease worldwide. microRNAs (miRNAs) have been reported to play essential roles in DN progression. However, the mechanism of miR-216a-5p on DN progression is still unclear.
methodsA DN model was established in human mesangial cells (HMC) by high glucose treatment. Cell proliferation was investigated using the cell counting kit-8 (CCK-8) assay. The cell cycle was measured through a propidium iodide (PI) cell cycle kit with flow cytometry. The interaction between miR-216a-5p and forkhead boxO1 (FoxO1) was probed by a bioinformatics analysis and luciferase activity assay. The expression of miR-216a-5p was detected using a quantitative real-time polymerase chain reaction (qRT-PCR). The abundances of FoxO1 and cell cycle-related cyclinD1, cyclin-dependent kinase 4 (CDK4), CDK6 and p27 were examined by qRT-PCR and Western blots (WB).
resultsmiR-216a-5p was up-regulated while FoxO1 was down-regulated in DN tissues. Moreover, miR-216a-5p promoted cell proliferation by regulating the cell cycle in high glucose-treated HMC cells. Notably, FoxO1 was a direct target and negatively correlated with miR-216a-5p. In addition, miR-216a induced cyclinD1, CDK4 and CDK6 but inhibited p27 expressions at the mRNA and protein levels. Furthermore, FoxO1 restoration reversed the regulatory effect of miR-216a on the cell cycle by regulating cyclinD1, CDK4, CDK6 and p27 abundances at the mRNA and protein levels.
conclusionmiR-216a-5p is ectopic in DN and it promotes cell proliferation through regulating the cell cycle by targeting FoxO1 in high glucose-stimulated HMC cells, indicating it may serve as a novel biomarker for DN treatment.
Indexed as
Identifiers
31933751PMC6944002W3010309610What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.