Heparin-Binding EGF-like Growth Factor Decreases Neutrophil-Endothelial Cell Interactions

Dorothy Rocourt, Veela B. Mehta, Dan Wu, Gail E. Besner

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background: Hyperadhesiveness of neutrophils (PMN) to vascular endothelial cells (EC) followed by neutrophil transendothelial migration play important roles in the initiation of ischemia/reperfusion (I/R)-mediated injury. We investigated whether the ability of heparin-binding EGF-like growth factor (HB-EGF) to decrease intestinal injury after intestinal I/R is mediated, in part, by its ability to affect PMN-EC interactions and EC junctional integrity. Materials and methods: Human umbilical vein EC monolayers were treated with HB-EGF (100 ng/mL) or phosphate-buffered saline followed by anoxia/reoxygenation (A/R). Simultaneously, labeled human PMN were treated with HB-EGF or phosphate-buffered saline and then co-incubated with EC for determination of PMN-EC adherence and PMN transendothelial migration. EC junctional integrity was also determined. Results: PMN-EC adhesion increased after exposure of EC to A/R compared to EC exposed to normoxia (87% versus 64% binding, P < 0.05, Wilcoxon rank sum test). A/R-induced PMN-EC hyperadherence was significantly decreased by treatment of PMN with HB-EGF compared to nontreated cells (51% versus 87% binding, P < 0.05). HB-EGF significantly decreased PMN transendothelial migration and also augmented EC tight junctional integrity after A/R. Conclusions: HB-EGF significantly reduces A/R-induced PMN-EC adhesion and PMN transendothelial migration and augments junctional integrity in vitro. Thus, HB-EGF acts not only as a potent cytoprotective agent for the intestine, but as an anti-inflammatory agent as well.

Original languageEnglish (US)
Pages (from-to)262-266
Number of pages5
JournalJournal of Surgical Research
Volume141
Issue number2
DOIs
StatePublished - Aug 1 2007

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Cell Communication
Neutrophils
Endothelial Cells
Transendothelial and Transepithelial Migration
Nonparametric Statistics
Cell Adhesion
Heparin-binding EGF-like Growth Factor
Phosphates
Human Umbilical Vein Endothelial Cells
Reperfusion Injury
Reperfusion
Intestines
Anti-Inflammatory Agents
Ischemia

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Rocourt, Dorothy ; Mehta, Veela B. ; Wu, Dan ; Besner, Gail E. / Heparin-Binding EGF-like Growth Factor Decreases Neutrophil-Endothelial Cell Interactions. In: Journal of Surgical Research. 2007 ; Vol. 141, No. 2. pp. 262-266.
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abstract = "Background: Hyperadhesiveness of neutrophils (PMN) to vascular endothelial cells (EC) followed by neutrophil transendothelial migration play important roles in the initiation of ischemia/reperfusion (I/R)-mediated injury. We investigated whether the ability of heparin-binding EGF-like growth factor (HB-EGF) to decrease intestinal injury after intestinal I/R is mediated, in part, by its ability to affect PMN-EC interactions and EC junctional integrity. Materials and methods: Human umbilical vein EC monolayers were treated with HB-EGF (100 ng/mL) or phosphate-buffered saline followed by anoxia/reoxygenation (A/R). Simultaneously, labeled human PMN were treated with HB-EGF or phosphate-buffered saline and then co-incubated with EC for determination of PMN-EC adherence and PMN transendothelial migration. EC junctional integrity was also determined. Results: PMN-EC adhesion increased after exposure of EC to A/R compared to EC exposed to normoxia (87{\%} versus 64{\%} binding, P < 0.05, Wilcoxon rank sum test). A/R-induced PMN-EC hyperadherence was significantly decreased by treatment of PMN with HB-EGF compared to nontreated cells (51{\%} versus 87{\%} binding, P < 0.05). HB-EGF significantly decreased PMN transendothelial migration and also augmented EC tight junctional integrity after A/R. Conclusions: HB-EGF significantly reduces A/R-induced PMN-EC adhesion and PMN transendothelial migration and augments junctional integrity in vitro. Thus, HB-EGF acts not only as a potent cytoprotective agent for the intestine, but as an anti-inflammatory agent as well.",
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Heparin-Binding EGF-like Growth Factor Decreases Neutrophil-Endothelial Cell Interactions. / Rocourt, Dorothy; Mehta, Veela B.; Wu, Dan; Besner, Gail E.

In: Journal of Surgical Research, Vol. 141, No. 2, 01.08.2007, p. 262-266.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Heparin-Binding EGF-like Growth Factor Decreases Neutrophil-Endothelial Cell Interactions

AU - Rocourt, Dorothy

AU - Mehta, Veela B.

AU - Wu, Dan

AU - Besner, Gail E.

PY - 2007/8/1

Y1 - 2007/8/1

N2 - Background: Hyperadhesiveness of neutrophils (PMN) to vascular endothelial cells (EC) followed by neutrophil transendothelial migration play important roles in the initiation of ischemia/reperfusion (I/R)-mediated injury. We investigated whether the ability of heparin-binding EGF-like growth factor (HB-EGF) to decrease intestinal injury after intestinal I/R is mediated, in part, by its ability to affect PMN-EC interactions and EC junctional integrity. Materials and methods: Human umbilical vein EC monolayers were treated with HB-EGF (100 ng/mL) or phosphate-buffered saline followed by anoxia/reoxygenation (A/R). Simultaneously, labeled human PMN were treated with HB-EGF or phosphate-buffered saline and then co-incubated with EC for determination of PMN-EC adherence and PMN transendothelial migration. EC junctional integrity was also determined. Results: PMN-EC adhesion increased after exposure of EC to A/R compared to EC exposed to normoxia (87% versus 64% binding, P < 0.05, Wilcoxon rank sum test). A/R-induced PMN-EC hyperadherence was significantly decreased by treatment of PMN with HB-EGF compared to nontreated cells (51% versus 87% binding, P < 0.05). HB-EGF significantly decreased PMN transendothelial migration and also augmented EC tight junctional integrity after A/R. Conclusions: HB-EGF significantly reduces A/R-induced PMN-EC adhesion and PMN transendothelial migration and augments junctional integrity in vitro. Thus, HB-EGF acts not only as a potent cytoprotective agent for the intestine, but as an anti-inflammatory agent as well.

AB - Background: Hyperadhesiveness of neutrophils (PMN) to vascular endothelial cells (EC) followed by neutrophil transendothelial migration play important roles in the initiation of ischemia/reperfusion (I/R)-mediated injury. We investigated whether the ability of heparin-binding EGF-like growth factor (HB-EGF) to decrease intestinal injury after intestinal I/R is mediated, in part, by its ability to affect PMN-EC interactions and EC junctional integrity. Materials and methods: Human umbilical vein EC monolayers were treated with HB-EGF (100 ng/mL) or phosphate-buffered saline followed by anoxia/reoxygenation (A/R). Simultaneously, labeled human PMN were treated with HB-EGF or phosphate-buffered saline and then co-incubated with EC for determination of PMN-EC adherence and PMN transendothelial migration. EC junctional integrity was also determined. Results: PMN-EC adhesion increased after exposure of EC to A/R compared to EC exposed to normoxia (87% versus 64% binding, P < 0.05, Wilcoxon rank sum test). A/R-induced PMN-EC hyperadherence was significantly decreased by treatment of PMN with HB-EGF compared to nontreated cells (51% versus 87% binding, P < 0.05). HB-EGF significantly decreased PMN transendothelial migration and also augmented EC tight junctional integrity after A/R. Conclusions: HB-EGF significantly reduces A/R-induced PMN-EC adhesion and PMN transendothelial migration and augments junctional integrity in vitro. Thus, HB-EGF acts not only as a potent cytoprotective agent for the intestine, but as an anti-inflammatory agent as well.

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