ArticleMolecular and cellular biochemistry2015
Roles of miRNA-24 in regulating endothelial nitric oxide synthase expression and vascular endothelial cell proliferation.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- MiRNA-based drugs: challenges and delivery strategies.Applied microbiology and biotechnology · 2025Review
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- MicroRNA-Mediated Regulation of Vascular Endothelium: From Pro-Inflammation to Atherosclerosis.International journal of molecular sciences · 2025Review
- The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Review
- Glycemia-Induced miRNA Changes: A Review.International journal of molecular sciences · 2023Review
- IL-1β promotes hypoxic vascular endothelial cell proliferation through the miR-24-3p/NKAP/NF-κB axis.Bioscience reports · 2022Article
- Endothelial Dysfunction Driven by Hypoxia-The Influence of Oxygen Deficiency on NO Bioavailability.Biomolecules · 2021Review
- Multifunctional Biodegradable Vascular PLLA Scaffold with Improved X-ray Opacity, Anti-Inflammation, and Re-Endothelization.Polymers · 2021Article
- MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy.Cardiovascular diabetology · 2020Review
- Article
- Identification of Immune Response to Sacbrood Virus Infection inFrontiers in genetics · 2020Article
- eNOS expression and NO release during hypoxia is inhibited by miR-200b in human endothelial cells.Angiogenesis · 2018Article
- microRNAs regulate nitric oxide release from endothelial cells by targeting NOS3.Journal of thrombosis and thrombolysis · 2018Article
- Next-generation sequencing-based microRNA profiling of mice testis subjected to transient heat stress.Oncotarget · 2017Article
- Low-density lipoprotein modified by myeloperoxidase oxidants induces endothelial dysfunction.Redox biology · 2017Article
- The Epigenetic Machinery in Vascular Dysfunction and Hypertension.Current hypertension reports · 2017Review
- Role of MicroRNA in Endothelial Dysfunction and Hypertension.Current hypertension reports · 2016Review
- miR-424-5p promotes proliferation of gastric cancer by targeting Smad3 through TGF-β signaling pathway.Oncotarget · 2016Article
- Posttranscriptional and transcriptional regulation of endothelial nitric-oxide synthase during hypoxia: the role of microRNAs.Cellular & molecular biology letters · 2016Review
- Function, Role, and Clinical Application of MicroRNAs in Vascular Aging.BioMed research international · 2016Review
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Authors and funding
7 authors.
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Abstract
This study is to investigate the effect of miRNA-24 on endothelial nitric oxide synthase (eNOS) expression and vascular endothelial cell proliferation. Constructed high expression miRNA-24 plasmids were introduced into human umbilical vein endothelial cells (HUVECs) by liposome. Cell numbers were counted by a Hemocytometer, and cell proliferation was detected by MTT assay. The expression levels of eNOS and specificity protein 1 (Sp1) at mRNA and protein levels were, respectively, examined by real-time PCR, immunohistochemistry, and Western blotting. Compared with the control group, endothelial cell proliferation in miRNA-24 group significantly decreased by 64.24 % (6.53 ± 0.11 vs 18.26 ± 0.45, P < 0.01). The expression of eNOS at mRNA and protein levels in miRNA-24 group decreased by 64.21 % (0.34 ± 0.01 vs 0.95 ± 0.02, P < 0.05) and 82.86 % (0.072 ± 0.06 vs 0.42 ± 0.06, P < 0.05), respectively. Meanwhile, the expression of Sp1 at mRNA and protein levels in miRNA-24 group decreased by 64.64 % (0.35 ± 0.01 vs 0.99 ± 0.03, P < 0.05) and 60.34 % (0.23 ± 0.05 vs 0.58 ± 0.07, P < 0.05), respectively. In anti-miRNA-24 group, endothelial cell proliferation decreased by 33.46 % compared with the control group (12.15 ± 0.21 vs 18.26 ± 0.45, P < 0.01), while it increased by 46.25 % compared with the miRNA-24 group (12.15 ± 0.21 vs 6.53 ± 0.11, P < 0.01). The expression of eNOS at mRNA and protein levels in anti-miRNA-24 group decreased by 44.21 % (0.53 ± 0.04 vs 0.95 ± 0.02, P < 0.05) and by 30.95 %(0.29 ± 0.05 vs 0.42 ± 0.06, P < 0.05) compared with the control group, while it increased by 35.84 % (0.53 ± 0.04 vs 0.34 ± 0.01, P < 0.05) and by 75.17 % (0.29 ± 0.05 vs 0.072 ± 0.06, P < 0.05) compared with miRNA-24 group. The expression of Sp1 at mRNA and protein levels in ant-miRNA-24 group decreased by 36.36 % (0.63 ± 0.04 vs 0.99 ± 0.03, P < 0.05) and by 22.41 % (0.45 ± 0.06 vs 0.58 ± 0.07, P < 0.05) compared with the control group, while it increased by 44.44 % (0.63 ± 0.04 vs 0.35 ± 0.01, P < 0.05) and by 48.88 % (0.45 ± 0.06 vs 0.23 ± 0.05, P < 0.05) compared with miRNA-24 group. HUVECs proliferation and eNOS expression are significantly inhibited by miRNA-24. Sp1, which is regulated by miRNA-24, might act as one of the important factors involved in eNOS gene expression.
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