ArticlePloS one2014
Regulation of coagulation factor XI expression by microRNAs in the human liver.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 37 citations in OpenAlex.
- Post-transcriptional control of haemostatic genes: mechanisms and emerging therapeutic concepts in thrombo-inflammatory disorders.Cardiovascular research · 2023Review
- PBMC MicroRNAs: Promising Biomarkers for the Differential Diagnosis of COVID-19 Patients with Abnormal Coagulation Indices.Current microbiology · 2023Article
- The Intricate Role of Non-Coding RNAs in Sepsis-Associated Disseminated Intravascular Coagulation.International journal of molecular sciences · 2023Review
- Research progress of NF-κB signaling pathway and thrombosis.Frontiers in immunology · 2023Review
- Role of microRNAs in Hemophilia and Thrombosis in Humans.International journal of molecular sciences · 2020Review
- Role of microRNAs in Venous Thromboembolism.International journal of molecular sciences · 2020Review
- MiR-23a-3p promoted G1/S cell cycle transition by targeting protocadherin17 in hepatocellular carcinoma.Journal of physiology and biochemistry · 2020Article
- Neutrophil extracellular trap components increase the expression of coagulation factors.Biomedical reports · 2019Article
- Regulation of TFPIα expression by miR-27a/b-3p in human endothelial cells under normal conditions and in response to androgens.Scientific reports · 2017Article
- Genome-wide association study with additional genetic and post-transcriptional analyses reveals novel regulators of plasma factor XI levels.Human molecular genetics · 2017Article
- Overexpression of miR-24 Is Involved in the Formation of Hypocoagulation State after Severe Trauma by Inhibiting the Synthesis of Coagulation Factor X.Disease markers · 2017Article
- Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
High levels of factor XI (FXI) increase the risk of thromboembolic disease. However, the genetic and environmental factors regulating FXI expression are still largely unknown. The aim of our study was to evaluate the regulation of FXI by microRNAs (miRNAs) in the human liver. In silico prediction yielded four miRNA candidates that might regulate FXI expression. HepG2 cells were transfected with miR-181a-5p, miR-23a-3p, miR-16-5p and miR-195-5p. We used mir-494, which was not predicted to bind to F11, as a negative control. Only miR-181a-5p caused a significant decrease both in FXI protein and F11 mRNA levels. In addition, transfection with a miR-181a-5p inhibitor in PLC/PRF/5 hepatic cells increased both the levels of F11 mRNA and extracellular FXI. Luciferase assays in human colon cancer cells deficient for Dicer (HCT-DK) demonstrated a direct interaction between miR-181a-5p and 3'untranslated region of F11. Additionally, F11 mRNA levels were inversely and significantly correlated with miR-181a-5p levels in 114 healthy livers, but not with miR-494. This study demonstrates that FXI expression is directly regulated by a specific miRNA, miR-181a-5p, in the human liver. Future studies are necessary to further investigate the potential consequences of miRNA dysregulation in pathologies involving FXI.
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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.