Phenotypic assessment of endothelial microparticles in patients with heart failure and after heart transplantation: Switch from cell activation to apoptosis

Santiago Garcia, Julio Chirinos, Javier Jimenez, Freddy Del Carpio Muñoz, Mariana Canoniero, Wenche Jy, Joaquin J Jimenez, Lawrence Horstman, Yeon Ahn

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Background: Endothelial microparticles (EMPs) are sub-microscopic membrane vesicles that are shed from the surface of endothelial cells during activation, injury and/or apoptosis. Endothelial cells release phenotypically and quantitatively distinct endothelial microparticles (EMPs) in activation and apoptosis. Therefore, the phenotypic assessment of EMPs can provide useful information reflecting the nature of endothelial injury. We tested the hypothesis that heart transplantation (HT) modifies the pattern of endothelial injury seen in patients with congestive heart failure (CHF). Methods: Flow cytometry was used to measure EMPs identified by E-selectin (CD62) and platelet-endothelial cell adhesion molecule 1 (CD31) in 23 patients with advanced heart failure and in 23 HT recipients. A cohort of 23 healthy individuals served as controls. Results: Heart failure patients were found to have significantly higher levels of EMP62E (577 counts/μl) than controls (192 counts/μl) and post-transplant patients (152 counts/μl) (p < 0.0001). Levels of endothelial microparticles expressing CD31 were significantly different among study groups (analysis of variance [ANOVA], p = 0.001). Heart failure patients had significantly higher levels (1,526 counts/μl) than controls (395 counts/μl) (p < 0.01). Levels of EMP31 remained elevated after heart transplant (935 counts/μl) (p = non-significant). The EMP62/EMP31 ratio, an index of activation (high ratio) or apoptosis (low ratio), was significantly different between the groups (ANOVA, p = 0.01). Post-transplant patients had significantly lower ratios (0.16) than CHF patients (0.38) and controls (0.49). Conclusions: Cardiac transplantation is associated with a different pattern of endothelial cell injury than that seen in heart failure. The phenotypic assessment of EMPs in post-transplant patients is consistent with increased apoptotic activity.

Original languageEnglish
Pages (from-to)2184-2189
Number of pages6
JournalJournal of Heart and Lung Transplantation
Volume24
Issue number12
DOIs
StatePublished - Dec 1 2005

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Heart Transplantation
Heart Failure
Apoptosis
Transplants
Endothelial Cells
Wounds and Injuries
Analysis of Variance
CD31 Antigens
E-Selectin
Flow Cytometry
Membranes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery
  • Transplantation

Cite this

Phenotypic assessment of endothelial microparticles in patients with heart failure and after heart transplantation : Switch from cell activation to apoptosis. / Garcia, Santiago; Chirinos, Julio; Jimenez, Javier; Del Carpio Muñoz, Freddy; Canoniero, Mariana; Jy, Wenche; Jimenez, Joaquin J; Horstman, Lawrence; Ahn, Yeon.

In: Journal of Heart and Lung Transplantation, Vol. 24, No. 12, 01.12.2005, p. 2184-2189.

Research output: Contribution to journalArticle

Garcia, Santiago ; Chirinos, Julio ; Jimenez, Javier ; Del Carpio Muñoz, Freddy ; Canoniero, Mariana ; Jy, Wenche ; Jimenez, Joaquin J ; Horstman, Lawrence ; Ahn, Yeon. / Phenotypic assessment of endothelial microparticles in patients with heart failure and after heart transplantation : Switch from cell activation to apoptosis. In: Journal of Heart and Lung Transplantation. 2005 ; Vol. 24, No. 12. pp. 2184-2189.
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abstract = "Background: Endothelial microparticles (EMPs) are sub-microscopic membrane vesicles that are shed from the surface of endothelial cells during activation, injury and/or apoptosis. Endothelial cells release phenotypically and quantitatively distinct endothelial microparticles (EMPs) in activation and apoptosis. Therefore, the phenotypic assessment of EMPs can provide useful information reflecting the nature of endothelial injury. We tested the hypothesis that heart transplantation (HT) modifies the pattern of endothelial injury seen in patients with congestive heart failure (CHF). Methods: Flow cytometry was used to measure EMPs identified by E-selectin (CD62) and platelet-endothelial cell adhesion molecule 1 (CD31) in 23 patients with advanced heart failure and in 23 HT recipients. A cohort of 23 healthy individuals served as controls. Results: Heart failure patients were found to have significantly higher levels of EMP62E (577 counts/μl) than controls (192 counts/μl) and post-transplant patients (152 counts/μl) (p < 0.0001). Levels of endothelial microparticles expressing CD31 were significantly different among study groups (analysis of variance [ANOVA], p = 0.001). Heart failure patients had significantly higher levels (1,526 counts/μl) than controls (395 counts/μl) (p < 0.01). Levels of EMP31 remained elevated after heart transplant (935 counts/μl) (p = non-significant). The EMP62/EMP31 ratio, an index of activation (high ratio) or apoptosis (low ratio), was significantly different between the groups (ANOVA, p = 0.01). Post-transplant patients had significantly lower ratios (0.16) than CHF patients (0.38) and controls (0.49). Conclusions: Cardiac transplantation is associated with a different pattern of endothelial cell injury than that seen in heart failure. The phenotypic assessment of EMPs in post-transplant patients is consistent with increased apoptotic activity.",
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T1 - Phenotypic assessment of endothelial microparticles in patients with heart failure and after heart transplantation

T2 - Switch from cell activation to apoptosis

AU - Garcia, Santiago

AU - Chirinos, Julio

AU - Jimenez, Javier

AU - Del Carpio Muñoz, Freddy

AU - Canoniero, Mariana

AU - Jy, Wenche

AU - Jimenez, Joaquin J

AU - Horstman, Lawrence

AU - Ahn, Yeon

PY - 2005/12/1

Y1 - 2005/12/1

N2 - Background: Endothelial microparticles (EMPs) are sub-microscopic membrane vesicles that are shed from the surface of endothelial cells during activation, injury and/or apoptosis. Endothelial cells release phenotypically and quantitatively distinct endothelial microparticles (EMPs) in activation and apoptosis. Therefore, the phenotypic assessment of EMPs can provide useful information reflecting the nature of endothelial injury. We tested the hypothesis that heart transplantation (HT) modifies the pattern of endothelial injury seen in patients with congestive heart failure (CHF). Methods: Flow cytometry was used to measure EMPs identified by E-selectin (CD62) and platelet-endothelial cell adhesion molecule 1 (CD31) in 23 patients with advanced heart failure and in 23 HT recipients. A cohort of 23 healthy individuals served as controls. Results: Heart failure patients were found to have significantly higher levels of EMP62E (577 counts/μl) than controls (192 counts/μl) and post-transplant patients (152 counts/μl) (p < 0.0001). Levels of endothelial microparticles expressing CD31 were significantly different among study groups (analysis of variance [ANOVA], p = 0.001). Heart failure patients had significantly higher levels (1,526 counts/μl) than controls (395 counts/μl) (p < 0.01). Levels of EMP31 remained elevated after heart transplant (935 counts/μl) (p = non-significant). The EMP62/EMP31 ratio, an index of activation (high ratio) or apoptosis (low ratio), was significantly different between the groups (ANOVA, p = 0.01). Post-transplant patients had significantly lower ratios (0.16) than CHF patients (0.38) and controls (0.49). Conclusions: Cardiac transplantation is associated with a different pattern of endothelial cell injury than that seen in heart failure. The phenotypic assessment of EMPs in post-transplant patients is consistent with increased apoptotic activity.

AB - Background: Endothelial microparticles (EMPs) are sub-microscopic membrane vesicles that are shed from the surface of endothelial cells during activation, injury and/or apoptosis. Endothelial cells release phenotypically and quantitatively distinct endothelial microparticles (EMPs) in activation and apoptosis. Therefore, the phenotypic assessment of EMPs can provide useful information reflecting the nature of endothelial injury. We tested the hypothesis that heart transplantation (HT) modifies the pattern of endothelial injury seen in patients with congestive heart failure (CHF). Methods: Flow cytometry was used to measure EMPs identified by E-selectin (CD62) and platelet-endothelial cell adhesion molecule 1 (CD31) in 23 patients with advanced heart failure and in 23 HT recipients. A cohort of 23 healthy individuals served as controls. Results: Heart failure patients were found to have significantly higher levels of EMP62E (577 counts/μl) than controls (192 counts/μl) and post-transplant patients (152 counts/μl) (p < 0.0001). Levels of endothelial microparticles expressing CD31 were significantly different among study groups (analysis of variance [ANOVA], p = 0.001). Heart failure patients had significantly higher levels (1,526 counts/μl) than controls (395 counts/μl) (p < 0.01). Levels of EMP31 remained elevated after heart transplant (935 counts/μl) (p = non-significant). The EMP62/EMP31 ratio, an index of activation (high ratio) or apoptosis (low ratio), was significantly different between the groups (ANOVA, p = 0.01). Post-transplant patients had significantly lower ratios (0.16) than CHF patients (0.38) and controls (0.49). Conclusions: Cardiac transplantation is associated with a different pattern of endothelial cell injury than that seen in heart failure. The phenotypic assessment of EMPs in post-transplant patients is consistent with increased apoptotic activity.

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