Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism

Julio A. Chirinos, Gustavo A. Heresi, Hermes Velasquez, Wenche Jy, Joaquin J Jimenez, Eugene Ahn, Lawrence L. Horstman, Andres O. Soriano, Juan P. Zambrano, Yeon Ahn

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Abstract

OBJECTIVES: The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). BACKGROUND: The details of interactions between endothelium, platelets, and leukocytes in VTE are not well understood. METHODS: We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b- (EMP31) or E-selectin (EMP62E); 2) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. RESULTS: Patients with VTE had marked elevations of EMP 31 (2,193 vs. 383 counts/μl; p = 0.003), EMP62E (368 vs. 223 counts/μl; p = 0.001), and EMP-monocyte conjugates (3.3% vs. 2.5%; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7% vs. 39.6%; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). CONCLUSIONS: Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation.

Original languageEnglish
Pages (from-to)1467-1471
Number of pages5
JournalJournal of the American College of Cardiology
Volume45
Issue number9
DOIs
StatePublished - May 3 2005

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Venous Thromboembolism
Platelet Activation
Leukocytes
Blood Platelets
Monocytes
P-Selectin
E-Selectin
Endothelium
Concept Formation
Flow Cytometry
Thrombosis
Fluorescence

ASJC Scopus subject areas

  • Nursing(all)

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Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism. / Chirinos, Julio A.; Heresi, Gustavo A.; Velasquez, Hermes; Jy, Wenche; Jimenez, Joaquin J; Ahn, Eugene; Horstman, Lawrence L.; Soriano, Andres O.; Zambrano, Juan P.; Ahn, Yeon.

In: Journal of the American College of Cardiology, Vol. 45, No. 9, 03.05.2005, p. 1467-1471.

Research output: Contribution to journalArticle

Chirinos, Julio A. ; Heresi, Gustavo A. ; Velasquez, Hermes ; Jy, Wenche ; Jimenez, Joaquin J ; Ahn, Eugene ; Horstman, Lawrence L. ; Soriano, Andres O. ; Zambrano, Juan P. ; Ahn, Yeon. / Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism. In: Journal of the American College of Cardiology. 2005 ; Vol. 45, No. 9. pp. 1467-1471.
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title = "Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism",
abstract = "OBJECTIVES: The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). BACKGROUND: The details of interactions between endothelium, platelets, and leukocytes in VTE are not well understood. METHODS: We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b- (EMP31) or E-selectin (EMP62E); 2) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. RESULTS: Patients with VTE had marked elevations of EMP 31 (2,193 vs. 383 counts/μl; p = 0.003), EMP62E (368 vs. 223 counts/μl; p = 0.001), and EMP-monocyte conjugates (3.3{\%} vs. 2.5{\%}; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7{\%} vs. 39.6{\%}; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). CONCLUSIONS: Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation.",
author = "Chirinos, {Julio A.} and Heresi, {Gustavo A.} and Hermes Velasquez and Wenche Jy and Jimenez, {Joaquin J} and Eugene Ahn and Horstman, {Lawrence L.} and Soriano, {Andres O.} and Zambrano, {Juan P.} and Yeon Ahn",
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T1 - Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism

AU - Chirinos, Julio A.

AU - Heresi, Gustavo A.

AU - Velasquez, Hermes

AU - Jy, Wenche

AU - Jimenez, Joaquin J

AU - Ahn, Eugene

AU - Horstman, Lawrence L.

AU - Soriano, Andres O.

AU - Zambrano, Juan P.

AU - Ahn, Yeon

PY - 2005/5/3

Y1 - 2005/5/3

N2 - OBJECTIVES: The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). BACKGROUND: The details of interactions between endothelium, platelets, and leukocytes in VTE are not well understood. METHODS: We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b- (EMP31) or E-selectin (EMP62E); 2) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. RESULTS: Patients with VTE had marked elevations of EMP 31 (2,193 vs. 383 counts/μl; p = 0.003), EMP62E (368 vs. 223 counts/μl; p = 0.001), and EMP-monocyte conjugates (3.3% vs. 2.5%; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7% vs. 39.6%; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). CONCLUSIONS: Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation.

AB - OBJECTIVES: The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). BACKGROUND: The details of interactions between endothelium, platelets, and leukocytes in VTE are not well understood. METHODS: We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b- (EMP31) or E-selectin (EMP62E); 2) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. RESULTS: Patients with VTE had marked elevations of EMP 31 (2,193 vs. 383 counts/μl; p = 0.003), EMP62E (368 vs. 223 counts/μl; p = 0.001), and EMP-monocyte conjugates (3.3% vs. 2.5%; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7% vs. 39.6%; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). CONCLUSIONS: Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation.

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