Related Experiment Video
Updated: Mar 13, 2026

18:30
RNA-seq Analysis of Transcriptomes in Thrombin-treated and Control Human Pulmonary Microvascular Endothelial Cells
Published on: February 13, 2013
22.5K
Thrombin Concentration Shapes Endothelial Extracellular Vesicle Profiles with Divergent Inflammatory Functions.
Madhura Chatterjee1, Shiva Keshava2, Prity Dhara1
1BRIC-National Institute of Biomedical Genomics, Kalyani, India.
Blood Advances
|March 11, 2026
Summary
Thrombin
Area of Science:
- Biochemistry
- Cell Biology
- Vascular Biology
Background:
- Thrombin regulates inflammation and vascular barrier function via protease-activated receptor 1.
- Thrombin exhibits concentration-dependent opposing effects: low concentrations are protective, while high concentrations are detrimental.
- Mechanisms underlying thrombin's dual actions remain unclear.
Purpose of the Study:
- To investigate the role of extracellular vesicles (EVs) and their microRNA (miR) cargo in mediating thrombin's concentration-dependent effects on endothelial cells.
- To elucidate the specific miRs involved and their molecular targets in regulating inflammation and vascular integrity.
Main Methods:
- Stimulation of endothelial cells with varying thrombin concentrations to induce EV release.
- Characterization of miR cargo within low- vs. high-thrombin-induced EVs.
- Functional assays using manipulated EVs (e.g., with anti-miRs or miR mimics) to confirm causal roles.
- Analysis of target gene regulation (USP7, SOCS1) and downstream signaling pathways (NF-kB, cytokine signaling).
Main Results:
- Thrombin stimulates EV release, with distinct miR profiles at low and high concentrations.
- Low-thrombin EVs deliver miR-409-5p, targeting USP7 to confer anti-inflammatory and barrier-protective effects.
- High-thrombin EVs deliver miR-155-5p, targeting SOCS1 to promote inflammation and barrier disruption.
- Experimental manipulation of these miRs confirmed their causal roles in mediating thrombin's opposing effects.
Conclusions:
- EV-associated miRs are key mediators of thrombin's concentration-dependent dual actions on vascular cells.
- miR-409-5p and miR-155-5p represent critical regulators of thrombin-induced inflammation and barrier function.
- Engineered EVs delivering specific miRs or anti-miRs hold therapeutic potential for inflammatory vascular diseases.
Related Concept Videos
Anticoagulant Drugs: Low-Molecular-Weight Heparins
2.2K
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
2.2K
Clot Retraction and Fibrinolysis
9.9K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
9.9K
Venous Thrombosis I: Introduction
618
Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
618
Intracellular Signaling Affects Focal Adhesions
3.8K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
3.8K
Extrinsic and Intrinsic Pathways of Hemostasis
14.6K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
14.6K
Venous Thrombosis III: Interprofessional Care
445
Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
445

