T cell-derived extracellular vesicles are elevated in essential HTN.
Sabrina La Salvia1, Luca Musante1, Joanne Lannigan2
1Division of Nephrology and Center for Immunity, Inflammation, and Regenerative Medicine, Department of Medicine, University of Virginia, Charlottesville, Virginia.
American Journal of Physiology. Renal Physiology
|October 5, 2020
Summary
Leukocyte-derived extracellular vesicles (EVs), particularly T cell-derived EVs, are elevated in angiotensin II-induced hypertension. These EVs in blood and kidneys may serve as biomarkers for hypertension and related organ damage.
Area of Science:
- Cardiovascular Research
- Immunology
- Cell Biology
Background:
- Extracellular vesicles (EVs) are key mediators of intercellular communication.
- Hypertension (HTN) pathogenesis involves immune system dysregulation, particularly in the kidney and vasculature.
- Immune cell-derived EVs may influence inflammation and HTN development.
Purpose of the Study:
- To investigate alterations in leukocyte-derived EVs in angiotensin II (ANG II)-induced hypertension.
- To identify specific subtypes of EVs involved in HTN pathogenesis.
- To explore the potential of EVs as biomarkers for HTN and end-organ damage.
Main Methods:
- An in vivo model of ANG II-induced hypertension was utilized.
- EVs were isolated from blood and kidney tissues after 4 weeks of ANG II treatment.
- Imaging Flow Cytometry and specific antibody panels characterized EV origin and counts (platelets, endothelial cells, leukocytes).
Main Results:
- Leukocyte-derived EVs (CD45+) were significantly elevated in circulation and kidney tissue in ANG II-induced HTN.
- T cell-derived EVs (CD3+) showed a marked increase in ANG II-induced HTN compared to controls.
- Elevated T cell-derived EVs strongly correlated with increased systolic blood pressure.
Conclusions:
- Leukocyte-derived EVs, especially T cell-derived EVs, are elevated in experimental hypertension.
- These EVs may play a role in HTN pathogenesis and inflammation.
- Circulating and kidney EVs could serve as sensitive biomarkers for HTN and associated end-organ damage.
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