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Updated: Feb 5, 2026
13:46
Phenotypic and Functional Characterization of Endothelial Colony Forming Cells Derived from Human Umbilical Cord Blood
Published on: April 13, 2012
16.7K
Endothelial Colony-Forming Cell Function Is Reduced During HIV Infection
Samir K Gupta1, Ziyue Liu2, Emily C Sims1
1Department of Medicine, Indiana University School of Medicine, Indianapolis.
The Journal of Infectious Diseases
|September 22, 2018
Summary
Plasma from untreated HIV patients impairs endothelial cell function, increasing cardiovascular disease risk. Treatment with antiretroviral therapy (ART) restores this function, suggesting inflammation plays a key role.
Area of Science:
- Cardiovascular disease research
- HIV/AIDS research
- Endothelial cell biology
Background:
- Human immunodeficiency virus (HIV) infection is linked to cardiovascular disease.
- Monocyte activation and subsequent endothelial dysfunction are potential mechanisms connecting HIV and cardiovascular issues.
Purpose of the Study:
- To investigate the impact of HIV infection and antiretroviral therapy (ART) on endothelial colony-forming cell (ECFC) function.
- To explore the relationship between monocyte activation and impaired vascular reparative potential in HIV-positive individuals.
Main Methods:
- Blood samples were collected from HIV-negative, HIV-positive untreated, and HIV-positive treated participants.
- Flow cytometry assessed ECFCs and monocyte proportions.
- IncuCyte live cell imaging evaluated ECFC capillary proliferative capacity using participant plasma.
Main Results:
- ECFC proliferation was significantly reduced in plasma from untreated HIV participants compared to uninfected or treated groups.
- Specific ECFC functional parameters were negatively correlated with intermediate monocytes and soluble CD163 in HIV-positive individuals.
- No significant difference in ECFC percentage was observed between groups.
Conclusions:
- Plasma from untreated HIV patients impairs cord blood ECFC proliferative capacity.
- Monocyte activation in HIV-positive individuals is associated with reduced ECFC function, suggesting a mechanism for increased cardiovascular risk.
- Antiretroviral therapy (ART) appears to mitigate these negative effects on vascular reparative potential.
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