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KLF11 Protects against Venous Thrombosis via Suppressing Tissue Factor Expression
Wenying Liang1,2, Haocheng Lu1, Jinjian Sun1
1Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, United States.
Thrombosis and Haemostasis
|August 24, 2021
Summary
Krüppel-like factor 11 (KLF11) protects against venous thrombosis by downregulating tissue factor (TF) expression. This finding reveals KLF11 as a potential therapeutic target for thrombosis treatment.
Area of Science:
- Molecular Biology
- Vascular Biology
- Thrombosis Research
Background:
- Krüppel-like factors (KLFs) are crucial for vascular homeostasis.
- KLF11 is known to inhibit endothelial activation and protect against stroke.
- The role of KLF11 in venous thrombosis was previously unexplored.
Purpose of the Study:
- To investigate the role of KLF11 in venous thrombosis.
- To elucidate the molecular mechanisms by which KLF11 influences thrombosis-related gene expression.
Main Methods:
- Utilized a stasis-induced murine deep vein thrombosis (DVT) model and cultured endothelial cells (ECs).
- Employed gain- and loss-of-function approaches to manipulate KLF11 expression.
- Conducted reporter gene assays, chromatin immunoprecipitation, and co-immunoprecipitation.
Main Results:
- KLF11 expression increased under prothrombotic conditions.
- KLF11 significantly downregulated tumor necrosis factor-α (TNF-α)-induced tissue factor (TF) gene transcription.
- KLF11 inhibited the binding of early growth response 1 (EGR1) to the TF gene promoter.
- Klf11 knockout mice exhibited increased susceptibility to DVT.
Conclusions:
- KLF11 plays a protective role against venous thrombosis.
- KLF11 downregulates TF gene transcription by inhibiting EGR1 binding to the TF promoter under prothrombotic conditions.
- KLF11 represents a potential molecular target for thrombosis treatment.
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