Anti-TNF-α antibody (infliximab) therapy supports the recovery of enos and VEGFR2 protein expression in endothelial cells

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Abstract

The aim of this study is to investigate the effect of sera obtained from patients of Crohn's disease treated by anti-TNF-α antibody (infliximab) on the expression of endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor receptor-2 (VEGFR2) protein in human umbilical vein endothelial cells (HUVEC) cultured in vitro. HUVEC was cultured in the presence of sera derived from patients before and after treatment, or from healthy individuals. Effects of sera on the expression of eNOS and VEGFR2 were monitored by determination of mRNA and protein levels using real time quantitative PCR and Western blot analysis, respectively. The serum of Crohn's patients contained elevated levels of TNF-α (34±1.80 pg/mL), which resulted in a decrease in the protein level of eNOS in HUVEC with a simultaneous induction of VEGFR2. Infliximab treatment normalized the expression level of these proteins by decreasing TNF-α level, particularly in those cases when clinical healing was also recorded, and it also conferred restitution of the level of angiogenic cytokines. Results suggest that altered angiogenesis possibly contributes to the initiation and perpetuation of inflammatory processes in Inflammatory Bowel Disease (IBD). Endothelial dysfunction, a selective feature of Crohn's disease is beneficially affected by intravascular TNF-α neutralization.

Original languageEnglish
Pages (from-to)323-335
Number of pages13
JournalInternational Journal of Immunopathology and Pharmacology
Volume24
Issue number2
Publication statusPublished - Apr 2011

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Vascular Endothelial Growth Factor Receptor-2
Nitric Oxide Synthase Type III
Anti-Idiotypic Antibodies
Human Umbilical Vein Endothelial Cells
Endothelial Cells
Serum
Crohn Disease
Proteins
Therapeutics
Inflammatory Bowel Diseases
Real-Time Polymerase Chain Reaction
Western Blotting
Cytokines
Messenger RNA
Infliximab

Keywords

  • Crohn's disease
  • eNOS
  • HUVEC
  • Inflammatory bowel disease
  • Infliximab
  • TNF-α
  • Vascular endothelial growth factor receptor-2

ASJC Scopus subject areas

  • Pharmacology
  • Immunology
  • Immunology and Allergy

Cite this

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title = "Anti-TNF-α antibody (infliximab) therapy supports the recovery of enos and VEGFR2 protein expression in endothelial cells",
abstract = "The aim of this study is to investigate the effect of sera obtained from patients of Crohn's disease treated by anti-TNF-α antibody (infliximab) on the expression of endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor receptor-2 (VEGFR2) protein in human umbilical vein endothelial cells (HUVEC) cultured in vitro. HUVEC was cultured in the presence of sera derived from patients before and after treatment, or from healthy individuals. Effects of sera on the expression of eNOS and VEGFR2 were monitored by determination of mRNA and protein levels using real time quantitative PCR and Western blot analysis, respectively. The serum of Crohn's patients contained elevated levels of TNF-α (34±1.80 pg/mL), which resulted in a decrease in the protein level of eNOS in HUVEC with a simultaneous induction of VEGFR2. Infliximab treatment normalized the expression level of these proteins by decreasing TNF-α level, particularly in those cases when clinical healing was also recorded, and it also conferred restitution of the level of angiogenic cytokines. Results suggest that altered angiogenesis possibly contributes to the initiation and perpetuation of inflammatory processes in Inflammatory Bowel Disease (IBD). Endothelial dysfunction, a selective feature of Crohn's disease is beneficially affected by intravascular TNF-α neutralization.",
keywords = "Crohn's disease, eNOS, HUVEC, Inflammatory bowel disease, Infliximab, TNF-α, Vascular endothelial growth factor receptor-2",
author = "I. Altorjay and Z. Ver{\'e}b and Z. Serfőző and I. Bacskai and R. B{\'a}tori and F. Erdődi and M. Udvardy and S. Sipka and A. L{\'a}nyi and E. Rajnavolgyi and K. Palatka",
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AU - Altorjay, I.

AU - Veréb, Z.

AU - Serfőző, Z.

AU - Bacskai, I.

AU - Bátori, R.

AU - Erdődi, F.

AU - Udvardy, M.

AU - Sipka, S.

AU - Lányi, A.

AU - Rajnavolgyi, E.

AU - Palatka, K.

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