ArticleMedical principles and practice : international journal of the Kuwait University, Health Science Centre2015
Cyclic Adenosine Monophosphate-Mediated Enhancement of Vascular Endothelial Growth Factor Released by Differentiated Human Monocytic Cells: The Role of Protein Kinase A.
Article in Medical principles and practice : international journal of the Kuwait University, Health Science Centre, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Adrenaline is a prominent driver of inflammatory responses following hypoglycaemia.Diabetologia · 2026Trial
- Forskolin Sensitizes Human Acute Myeloid Leukemia Cells to H3K27me2/3 Demethylases GSKJ4 Inhibitor via Protein Kinase A.Frontiers in pharmacology · 2018Article
- Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections.Frontiers in immunology · 2018Review
- Efficacy of Rhodamine Light in the Treatment of Superficial Vascular Lesions of the Face.Medical principles and practice : international journal of the Kuwait University, Health Science CentreArticle
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOur investigation was designed to examine the signaling pathway involved in the enhancement of vascular endothelial growth factor (VEGF) release by β-adrenoceptor agonists. MATERIALS AND
methodsHuman U937 cells differentiated into macrophages were primed with lipopolysaccharide (LPS) in the absence or presence of β-adrenoceptor agonists and antagonists. The VEGF released and the intracellular cyclic adenosine monophosphate (cAMP) generated were assayed by ELISA. Where necessary, differences between mean values were tested for significance using Student's t test.
resultsIsoprenaline, procaterol and salbutamol concentration-dependently enhanced the release of VEGF induced by LPS in U937 cells. R*,R*-(±)-4-[2-[(2-(3-chlorophenyl)-2-hydroxyethyl)amino]propyl]phenoxyacetic acid (BRL 37344), a selective β3-adrenoceptor agonist, did not enhance VEGF release. Using isoprenaline as an agonist, propranolol, ICI 118551 and atenolol produced a parallel rightward shift of the concentration-response curve with no reduction in the maximum response. The -logKB values were 8.12 ± 0.17, 8.03 ± 0.05 and 7.23 ± 0.05 for propranolol, ICI 118551 and atenolol, respectively, indicating the possible involvement of both β1- and β2-adrenoceptor subtypes. Isoprenaline and prostaglandin E2 concentration-dependently increased cAMP generation in U937 cells. Isoprenaline, db-cAMP and 6-Bnz-cAMP, a protein kinase A (PKA) activator, all enhanced VEGF release induced by LPS, and this effect was abolished by KT 5720 and Rp-cAMPS, which are both selective PKA inhibitors, suggesting that PKA is the downstream effector of cAMP activity. 8-CPT-cAMP, a selective activator of the Epac system, had no effect on VEGF release induced by LPS, indicating that the Epac pathway played no role in the release process.
conclusionIn this study, we established that β1- and β2- but not β3-adrenoceptors mediated cAMP-dependent enhancement of VEGF release induced by LPS in differentiated U937 cells, and that PKA was the downstream effector of cAMP activity.
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