Vascular miR-181b controls tissue factor-dependent thrombogenicity and inflammation in type 2 diabetes
Open accessAbstract
Background: Diabetes mellitus is characterized by chronic vascular inflammation leading to pathological expression of the thrombogenic full length (fl) tissue factor (TF) and its isoform alternatively-spliced (as) TF. Blood-borne TF promotes factor (F) Xa generation resulting in a pro-thrombotic state and cardiovascular complications. MicroRNA (miR)s impact gene expression on the post-transcriptional level and contribute to vascular homeostasis. Their distinct role in the control of the diabetes-related procoagulant state remains poorly understood. Methods: In a cohort of patients with poorly controlled type 2 diabetes (n = 46) plasma levels of miR-181b were correlated with TF pathway activity and markers for vascular inflammation. In vitro, human microvascular endothelial cells (HMEC)-1 and human monocytes (THP-1) were transfected with miR-181b or anti-miR-181b and exposed to tumor necrosis factor (TNF) α or lipopolysaccharides (LPS). Expression of TF isoforms, vascular adhesion molecule (VCAM) 1 and nuclear factor (NF) κB nuclear translocation was assessed. Moreover, aortas, spleen, plasma, and bone marrow-derived macrophage (BMDM)s of mice carrying a deletion of the first miR-181b locus were analyzed with respect to TF expression and activity. Results: In patients with type 2 diabetes, plasma miR-181b negatively correlated with the procoagulant state as evidenced by TF protein, TF activity, d-dimer levels as well as markers for vascular inflammation. In HMEC-1, miR-181b abrogated TNFα-induced expression of flTF, asTF, and VCAM1. These results were validated using the anti-miR-181b. Mechanistically, we confirmed a miR-181b-mediated inhibition of importin-α3 (KPNA4) leading to reduced nuclear translocation of the TF transcription factor NFκB. In THP-1, miR-181b reduced both TF isoforms and FXa generation in response to LPS due to targeting phosphatase and tensin homolog (PTEN), a principal inducer for TF in monocytes. Moreover, in miR-181−/− animals, we found that reduced levels of miR-181b were accompanied by increased TF, VCAM1, and KPNA4 expression in aortic tissue as well as increased TF and PTEN expression in spleen. Finally, BMDMs of miR-181−/− mice showed increased TF expression and FXa generation upon stimulation with LPS. Conclusions: miR-181b epigenetically controls the procoagulant state in diabetes. Reduced miR-181b levels contribute to increased thrombogenicity and may help to identify individuals at particular risk for thrombosis.
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Vascular tissue factor promotes thrombosis and vascular inflammation, particularly in patients with type 2 diabetes who have higher levels of circulating trimethylamine N-oxide.
“Vascular TF promotes thrombosis and vascular inflammation123, particularl y in patients with type 2 diabetes who have higher levels of circulating TMAO124–126.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [124]
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- Authors
- Witkowski, M., Witkowski, M., Saffarzadeh, M., Friebel, J., Tabaraie, T., Ta Bao, L., Chakraborty, A., Dörner, A., Stratmann, B., Tschoepe, D., Winter, S. J., Krueger, A., Ruf, W., Landmesser, U., & Rauch, U.
- Affiliations
- Johannes Gutenberg University Mainz (DE)
- University Medical Center of the Johannes Gutenberg University Mainz (DE)
- Stiftung Charité (DE)
- Heart and Diabetes Center North Rhine-Westphalia (DE)
- Goethe University Frankfurt (DE)
- Corresponding author
- Rauch, Ursula
- ORCID
- Venue
- Cardiovascular Diabetology
- Published
- 2020-02-17
- Volume
- 19
- Issue
- 1
- Pages
- 20-20
- ISSN
- 1475-2840 (ISSN-L)
- PMC
- PMC7027062
- OpenAlex
- W3008078903
- Cited by
- 50
- References
- 44
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 8 · 2023: 12 · 2022: 7 · 2021: 13 · 2020: 4
- FWCI
- 3.16
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cardiovascular Diabetology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Refubium (Universitätsbibliothek der Freien Universität Berlin) (submittedVersion, cc-by)
- Universitätsbibliothek der FU Berlin Hochschulschriftenstelle u. Dokumentenserver (cc-by)
- Funders
- Deutsche Forschungsgemeinschaft (RA 799/5-1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Blood properties and coagulation
- Keywords
- miR-181b, type 2 diabetes, tissue factor, thrombogenicity, vascular inflammation, procoagulant state, importin alpha3, KPNA4, NF-κB nuclear translocation, PTEN, VCAM-1, factor Xa, microvascular endothelial cells, monocytes, D-dimer
- MeSH terms
- THP-1 Cells, Aged, Animals, Blood Coagulation, Diabetes Mellitus, Type 2, Female, Fibrin Fibrinogen Degradation Products, Humans, Inflammation, Male, Middle Aged, Thromboplastin, Thrombosis, Signal Transduction, Down-Regulation, NF-kappa B, Mice, Knockout, Vascular Cell Adhesion Molecule-1, alpha Karyopherins, MicroRNAs, Endothelial Cells, PTEN Phosphohydrolase
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