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Endothelium-derived microparticles inhibit human cardiac valve endothelial cell function
Denise B Klinkner1, John C Densmore, Sushma Kaul
1Department of Surgery, Division of Pediatric Surgery, Medical College of Wisconsin and Children's Research Institute, Milwaukee, WI 53226, USA.
Shock (Augusta, Ga.)
|May 25, 2006
Summary
Elevated endothelium-derived microparticles (EMPs) impair heart valve endothelial cell (EC) repair. This study shows EMPs inhibit EC proliferation and migration, suggesting a role in valvular injury during critical illness.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Biology
- Critical Care Medicine
Background:
- Elevated circulating endothelium-derived microparticles (EMPs) are linked to critical illnesses and vascular dysfunction.
- Cardiac valve injury involves endothelial dysfunction, but the role of EMPs is unclear.
Purpose of the Study:
- To investigate the hypothesis that circulating EMPs negatively regulate valvular endothelial cell (EC) proliferation and migration.
- To elucidate the mechanisms of endothelial dysfunction in cardiac valve injury.
Main Methods:
- EMPs were generated from stimulated human umbilical vein endothelial cells (HUVECs).
- Human mitral valve endothelial cells (HMVECs) were isolated and treated with EMPs.
- Proliferation (H-thymidine incorporation) and migration assays were performed with and without growth factors.
Main Results:
- EMPs inhibited HMVEC proliferation at high doses but stimulated HUVEC proliferation.
- EMPs suppressed basic fibroblast growth factor- and vascular endothelial growth factor-induced proliferation and migration in HMVECs.
- EMPs demonstrated dose-dependent regulation of valvular EC proliferation and modulated growth factor signaling.
Conclusions:
- Circulating EMPs may contribute to endothelial dysfunction in critical illnesses.
- EMPs play a potential role in valvular leaflet injury by inhibiting EC repair mechanisms.