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Circulating progenitor and mature endothelial cells in deep vein thrombosis
Aline M Alessio1, Miriam P Beltrame, Mariane C Flores Nascimento
11. Hematology and Hemotherapy Center, University of Campinas, Campinas-SP, Brazil.
Insights
Circulating endothelial cells (CEC) and progenitor cells (EPC) increase after deep vein thrombosis (DVT). These cells may play a role in DVT repair, with distinct release patterns observed in experimental and human studies.
Area of Science:
- Vascular Biology
- Hematology
- Cellular Biology
Background:
- Mature circulating endothelial cells (CEC) and circulating endothelial progenitor cells (EPC) are linked to endothelial injury.
- The involvement of CEC and EPC in deep vein thrombosis (DVT) remains unevaluated.
Purpose of the Study:
- To investigate the time course of CEC and EPC release following experimental DVT in mice.
- To assess the presence of CEC and EPC in patients with DVT during acute and chronic phases.
Main Methods:
- Utilized the FeCl3 model for experimental DVT induction in mice.
- Employed Flow Cytometry to quantify CEC and EPC levels in both murine models and human DVT patients.
- Analyzed cell counts in acute and chronic DVT patient phases, as well as serial samples over time.
Main Results:
- In mice, CEC and EPC levels elevated 24 hours post-DVT induction, peaking at 48 hours.
- CEC counts declined sharply after 72 hours, while EPC counts showed a less substantial decrease.
- DVT patients exhibited significantly increased CEC counts during both acute and chronic phases compared to healthy controls.
Conclusions:
- Findings suggest CEC and EPC participate in DVT repair processes at both early and late stages.
- Differential kinetics of CEC and EPC release indicate distinct roles in post-DVT reparative events.
- Elevated CEC levels in chronic DVT patients warrant further investigation into their long-term implications.
Introduction:
Mature circulating endothelial cells (CEC) and circulating endothelial progenitor cells (EPC) have been described in several conditions associated with endothelial injury. Their role in deep vein thrombosis (DVT) has not been previously evaluated.
Patients And Methods:
In this pilot study we evaluated the time course of CEC and EPC release after vena cava experimental DVT in mice, using the FeCl3 model. We also evaluated their presence in patients with DVT at different phases of the disease (acute and chronic phase). CEC and EPC were evaluated by Flow Cytometry.
Results:
In mice, both CEC and EPC were increased 24 hours after DVT induction, peaking 48 hours thereafter. After 72 hours, CEC counts decreased sharply, whereas EPC counts decreased less substantially. In DVT patients we observed a significant increase in CEC counts immediately after DVT compared to healthy individuals. Patients with chronic disease also presented a significant elevation of these cell count. In a subgroup of patients for whom serial samples were available, CEC counts decreased significantly after 9-15 months of the acute event.
Conclusions:
Our results suggest the participation of these cells in the reparative processes that follows DVT, both at immediate and late time-points. The different kinetics of CEC and EPC release in experimental DVT suggests a heterogeneous role for these cells in the reparative events after DVT.
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