ArticleScientific reports2017
Regulation of TFPIα expression by miR-27a/b-3p in human endothelial cells under normal conditions and in response to androgens.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Venous thrombosis unchained: Pandora's box of noninflammatory mechanisms.Blood advances · 2025Review
- Current landscape of exosomal non-coding RNAs in prostate cancer: Modulators and biomarkers.Non-coding RNA research · 2024Review
- Post-transcriptional control of haemostatic genes: mechanisms and emerging therapeutic concepts in thrombo-inflammatory disorders.Cardiovascular research · 2023Review
- Circulating MicroRNAs for Diagnosis of Acute Pulmonary Embolism: Still a Long Way to Go.BioMed research international · 2022Review
- Knockdown screening of chromatin binding and regulatory proteins in zebrafish identified Suz12b as a regulator of tfpia and an antithrombotic drug target.Scientific reports · 2021Article
- Role of microRNAs in Hemophilia and Thrombosis in Humans.International journal of molecular sciences · 2020Review
- Role of microRNAs in the Development of Cardiovascular Disease in Systemic Autoimmune Disorders.International journal of molecular sciences · 2020Review
- Androgen-Regulated microRNAs (AndroMiRs) as Novel Players in Adipogenesis.International journal of molecular sciences · 2019Review
- Neutrophil extracellular trap components increase the expression of coagulation factors.Biomedical reports · 2019Article
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increased risk of cardiovascular events in older men is multifactorial, but the significant reduction of testosterone levels has been involved. As this hormone regulates the expression of TFPI by unknown mechanisms, we aimed to evaluate the role of miRNAs in the regulation of TFPIα expression under normal conditions and in response to androgens. In silico studies allowed the selection of 4 miRNAs as potential TFPIα regulators. Only miR-27a/b-3p significantly reduced TFPIα expression in two endothelial cell lines. Luciferase assays demonstrated a direct interaction between miR-27a/b-3p and TFPI 3'UTR. Ex vivo analysis of TFPI and miRNA levels in 74 HUVEC samples from healthy subjects, showed a significant and inverse correlation between TFPI and miR-27a-3p. Moreover, anticoagulant activity of TFPIα from cells supernatants decreased ~30% with miR-27a/b-3p and increased ~50% with anti-miR-27a/b-3p. Interestingly, treatment of EA.hy926 with a physiological dose of dihydrotestosterone (30 nM) significantly increased (~40%) TFPIα expression with a parallel decreased (~50%) of miR-27a/b-3p expression. In concordance, increased levels of miR-27a/b-3p normalized the up-regulation induced by testosterone. Our results suggest that testosterone is a hinge in miR-27/TFPIα regulation axis. Future studies are needed to investigate whether testosterone variations are involved in a miR-27/TFPIα dysregulation that could increase the cardiovascular risk.
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