Cholecystokinin B Receptor from Human Jurkat Lymphoblastic T Cells Is Involved in Activator Protein-1-Responsive Gene Activation

Autor: Patrick Eldin, M F Lignon, Catherine Oiry, Gilbert Bergé, D. Gagne, Martine Le Cunff, Éric Cottin, Jean Martinez, N Bernad, J. C. Galleyrand, Pascal Clerc, Daniel Fourmy, Jean J. Leger
Přispěvatelé: Laboratoire des Amino-acides Peptides et Protéines (LAPP), Centre National de la Recherche Scientifique (CNRS)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Montpellier 1 (UM1), Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM), Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie et pharmacologie cellulaires et moléculaires, Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM), Géographie-cités (GC (UMR_8504)), Université Paris 1 Panthéon-Sorbonne (UP1)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Biologie et pathologie digestive, Institut Louis Bugnard-Institut National de la Santé et de la Recherche Médicale (INSERM)
Jazyk: angličtina
Rok vydání: 1997
Předmět:
Transcriptional Activation
Transcription
Genetic

medicine.drug_class
T-Lymphocytes
Biology
Ligands
Jurkat cells
Binding
Competitive

Sincalide
Cell Line
03 medical and health sciences
Jurkat Cells
0302 clinical medicine
Epidermal growth factor
medicine
Animals
Humans
Cloning
Molecular

Receptor
ComputingMilieux_MISCELLANEOUS
030304 developmental biology
Pharmacology
Regulation of gene expression
0303 health sciences
Reporter gene
Activator (genetics)
[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry
Molecular Biology/Molecular biology

Transfection
Receptor antagonist
Molecular biology
Gene Expression Regulation
Neoplastic

Transcription Factor AP-1
COS Cells
Molecular Medicine
Interleukin-2
Receptors
Cholecystokinin

hormones
hormone substitutes
and hormone antagonists

030217 neurology & neurosurgery
Cell Division
Zdroj: Molecular Pharmacology
Molecular Pharmacology, American Society for Pharmacology and Experimental Therapeutics, 1997, 52 (2), pp.292-299. ⟨10.1124/mol.52.2.292⟩
ResearcherID
Scopus-Elsevier
ISSN: 0026-895X
DOI: 10.1124/mol.52.2.292⟩
Popis: The aim of this study was to analyze the role of cholecystokinin (CCK(B)) receptor in human lymphoblastic Jurkat T cells. We investigated the trophic effect resulting from activation of such a receptor by using the reporter gene strategy. For this purpose, we transiently transfected Jurkat T cells with the reporter plasmid p[(TRE)3-tk-Luc] and found that CCK-8 was able to dose-dependently induce luciferase expression related to activator protein-1 (AP-1) activation with a maximal response identical to that obtained with compounds known to activate AP-1 complex (quantitatively, the same level of induction was obtained with 1 nM 12-O-tetradecanoylphorbol-13-acetate, 100 microM diacylglycerol, or 4 nM epidermal growth factor). The involvement of the CCK(B) receptor in such a stimulation was demonstrated by the inhibiting effect of the selective CCK(B) receptor antagonist PD-135,158. This effect was confirmed in COS-7 cells transfected with the cDNA of CCK(B) receptor cloned from Jurkat T cells. To better understand the AP-1-dependent luciferase expression in Jurkat T cells, we tested two specific inhibitors of serine/threonine phosphatases-1 and -2A: okadaic acid and calyculin A. These compounds strongly increased the phorbol-12-myristate-13-acetate response, whereas we have not observed a contribution of phosphatase inhibitors on a CCK-8-induced luciferase activity. To confirm that CCK(B) receptors are involved in AP-1 response, we investigated the CCK-8 effect on interleukin-2 expression, a natural endogenous gene regulated by several factors, including AP-1. In Jurkat T cells activated by phorbol-12-myristate-13-acetate and phytohemagglutinin, CCK-8 induced IL-2 expression. This induction was abolished by PD-135,158. Our results indicate that CCK-8 exerts a trophic effect in Jurkat T cells through stimulation of CCK(B) receptors by modulation of expression of AP-1-regulated genes.
Databáze: OpenAIRE