Beta-adrenergic receptor agonists induce the release of granulocyte chemotactic protein-2, oncostatin M, and vascular endothelial growth factor from macrophages

K.C.M. Verhoeckx, R.P. Doornbos, R.F. Witkamp, J. de Greef, R.J.T. Rodenburg

Research output: Contribution to journalArticleAcademicpeer-review

23 Citations (Scopus)

Abstract

Vascular endothelial growth factor (VEGF), oncostatin M (OSM), and granulocyte chemotactic protein-2 (GCP-2/CXCL6) are up-regulated in U937 macrophages and peripheral blood macrophages exposed to LPS, beta-adrenergic receptor (ß2-AR) agonists (e.g. zilpaterol, and clenbuterol) and some other agents that induce intracellular cAMP (prostaglandin E2, forskolin, and butyryl cAMP). LPS in combination with ß2-agonists and cAMP elevating agents had an additional effect on the release of VEGF, OSM, and CXCL6. These proteins are up-regulated after 16–24 h of exposure and this is mediated by the ß2-AR, as determined by time course experiments and the use of a specific ß2-AR antagonist (ICI 118551). Beta2-AR agonists are used as bronchodilators in the treatment of asthma, but appear to have no effect on the chronic inflammation of the disease. However, the up-regulation of VEGF, OSM, and CXCL6 may have adverse effects on the inflammatory process of asthma. These mediators are involved in the recruitment of neutrophils, airway remodelling and angiogenesis, known features of chronic inflammatory diseases. We propose that the up-regulation of these proteins could play a role in the adverse effects of prolonged excessive usage of ß2-AR agonists on the airways besides the desensitization of the ß2-AR
Original languageEnglish
Pages (from-to)1-7
JournalInternational Immunopharmacology
Volume6
Issue number1
DOIs
Publication statusPublished - 2006

Fingerprint

Chemokine CXCL6
Oncostatin M
Adrenergic beta-Agonists
Vascular Endothelial Growth Factor A
Macrophages
Adrenergic beta-2 Receptor Agonists
Chronic Disease
Up-Regulation
Asthma
Clenbuterol
Airway Remodeling
Neutrophil Infiltration
Bronchodilator Agents
Colforsin
Dinoprostone
Proteins
Inflammation

Keywords

  • nitric-oxide production
  • cyclic-amp
  • cell-line
  • modulation
  • cytokine
  • combination
  • transcriptomics
  • expression
  • proteomics
  • pathways

Cite this

@article{8743401b91b54fac95963f0a1b6f6488,
title = "Beta-adrenergic receptor agonists induce the release of granulocyte chemotactic protein-2, oncostatin M, and vascular endothelial growth factor from macrophages",
abstract = "Vascular endothelial growth factor (VEGF), oncostatin M (OSM), and granulocyte chemotactic protein-2 (GCP-2/CXCL6) are up-regulated in U937 macrophages and peripheral blood macrophages exposed to LPS, beta-adrenergic receptor ({\ss}2-AR) agonists (e.g. zilpaterol, and clenbuterol) and some other agents that induce intracellular cAMP (prostaglandin E2, forskolin, and butyryl cAMP). LPS in combination with {\ss}2-agonists and cAMP elevating agents had an additional effect on the release of VEGF, OSM, and CXCL6. These proteins are up-regulated after 16–24 h of exposure and this is mediated by the {\ss}2-AR, as determined by time course experiments and the use of a specific {\ss}2-AR antagonist (ICI 118551). Beta2-AR agonists are used as bronchodilators in the treatment of asthma, but appear to have no effect on the chronic inflammation of the disease. However, the up-regulation of VEGF, OSM, and CXCL6 may have adverse effects on the inflammatory process of asthma. These mediators are involved in the recruitment of neutrophils, airway remodelling and angiogenesis, known features of chronic inflammatory diseases. We propose that the up-regulation of these proteins could play a role in the adverse effects of prolonged excessive usage of {\ss}2-AR agonists on the airways besides the desensitization of the {\ss}2-AR",
keywords = "nitric-oxide production, cyclic-amp, cell-line, modulation, cytokine, combination, transcriptomics, expression, proteomics, pathways",
author = "K.C.M. Verhoeckx and R.P. Doornbos and R.F. Witkamp and {de Greef}, J. and R.J.T. Rodenburg",
year = "2006",
doi = "10.1016/j.intimp.2005.05.013",
language = "English",
volume = "6",
pages = "1--7",
journal = "International Immunopharmacology",
issn = "1567-5769",
publisher = "Elsevier",
number = "1",

}

Beta-adrenergic receptor agonists induce the release of granulocyte chemotactic protein-2, oncostatin M, and vascular endothelial growth factor from macrophages. / Verhoeckx, K.C.M.; Doornbos, R.P.; Witkamp, R.F.; de Greef, J.; Rodenburg, R.J.T.

In: International Immunopharmacology, Vol. 6, No. 1, 2006, p. 1-7.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Beta-adrenergic receptor agonists induce the release of granulocyte chemotactic protein-2, oncostatin M, and vascular endothelial growth factor from macrophages

AU - Verhoeckx, K.C.M.

AU - Doornbos, R.P.

AU - Witkamp, R.F.

AU - de Greef, J.

AU - Rodenburg, R.J.T.

PY - 2006

Y1 - 2006

N2 - Vascular endothelial growth factor (VEGF), oncostatin M (OSM), and granulocyte chemotactic protein-2 (GCP-2/CXCL6) are up-regulated in U937 macrophages and peripheral blood macrophages exposed to LPS, beta-adrenergic receptor (ß2-AR) agonists (e.g. zilpaterol, and clenbuterol) and some other agents that induce intracellular cAMP (prostaglandin E2, forskolin, and butyryl cAMP). LPS in combination with ß2-agonists and cAMP elevating agents had an additional effect on the release of VEGF, OSM, and CXCL6. These proteins are up-regulated after 16–24 h of exposure and this is mediated by the ß2-AR, as determined by time course experiments and the use of a specific ß2-AR antagonist (ICI 118551). Beta2-AR agonists are used as bronchodilators in the treatment of asthma, but appear to have no effect on the chronic inflammation of the disease. However, the up-regulation of VEGF, OSM, and CXCL6 may have adverse effects on the inflammatory process of asthma. These mediators are involved in the recruitment of neutrophils, airway remodelling and angiogenesis, known features of chronic inflammatory diseases. We propose that the up-regulation of these proteins could play a role in the adverse effects of prolonged excessive usage of ß2-AR agonists on the airways besides the desensitization of the ß2-AR

AB - Vascular endothelial growth factor (VEGF), oncostatin M (OSM), and granulocyte chemotactic protein-2 (GCP-2/CXCL6) are up-regulated in U937 macrophages and peripheral blood macrophages exposed to LPS, beta-adrenergic receptor (ß2-AR) agonists (e.g. zilpaterol, and clenbuterol) and some other agents that induce intracellular cAMP (prostaglandin E2, forskolin, and butyryl cAMP). LPS in combination with ß2-agonists and cAMP elevating agents had an additional effect on the release of VEGF, OSM, and CXCL6. These proteins are up-regulated after 16–24 h of exposure and this is mediated by the ß2-AR, as determined by time course experiments and the use of a specific ß2-AR antagonist (ICI 118551). Beta2-AR agonists are used as bronchodilators in the treatment of asthma, but appear to have no effect on the chronic inflammation of the disease. However, the up-regulation of VEGF, OSM, and CXCL6 may have adverse effects on the inflammatory process of asthma. These mediators are involved in the recruitment of neutrophils, airway remodelling and angiogenesis, known features of chronic inflammatory diseases. We propose that the up-regulation of these proteins could play a role in the adverse effects of prolonged excessive usage of ß2-AR agonists on the airways besides the desensitization of the ß2-AR

KW - nitric-oxide production

KW - cyclic-amp

KW - cell-line

KW - modulation

KW - cytokine

KW - combination

KW - transcriptomics

KW - expression

KW - proteomics

KW - pathways

U2 - 10.1016/j.intimp.2005.05.013

DO - 10.1016/j.intimp.2005.05.013

M3 - Article

VL - 6

SP - 1

EP - 7

JO - International Immunopharmacology

JF - International Immunopharmacology

SN - 1567-5769

IS - 1

ER -