title: Human H9 cells proliferation is differently controlled by vasoactive intestinal peptide or peptide histidine methionine: implication of a GTP-insensitive form of VPAC1 receptor.
abstract: The proliferation of human lymphoblastoma cell line (H9) was differently stimulated by Peptide Histidine Methionine (PHM) and Vasoactive Intestinal Peptide (VIP). PHM induced a cyclic AMP (cAMP) accumulation, abolished by Adenylate Cyclase (AC) inhibitors leading to a loss of proliferative effect. VIP mitogenic activity was Pertussis toxin (PTX) sensitive and AC inhibitors insensitive. Pharmacological experiments performed on H9 membranes with or without a GTP analogue indicated expression of both GTP-insensitive and -sensitive PHM/VIP high-affinity binding sites (HA). H9 cells expressed only the VPAC1 receptor. VIP(10-28), known as a VPAC1 antagonist, bond to all GTP-insensitive PHM sites and inhibited evenly the PHM and VIP mitogenic actions. These data strongly suggested different mechanisms initiated by VIP and PHM and highlighted the key role of GTP-insensitive binding sites in the control of cell proliferation.
authors.affiliation: IPBC CNRS-UMR 6187 Pôle Biologie Santé, 40 avenue du Recteur Pineau, 86022 Poitiers, France.
authors.forename: Stephanie
authors.initials: S
authors.lastname: Goursaud
authors.forename: Nicolas
authors.initials: N
authors.lastname: Pineau
authors.forename: Laetitia
authors.initials: L
authors.lastname: Becq-Giraudon
authors.forename: Pierre
authors.initials: P
authors.lastname: Gressens
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Muller
authors.forename: Thierry
authors.initials: T
authors.lastname: Janet
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000067956:Adenylyl Cyclase Inhibitors; D000704:Analysis of Variance; D015139:Blotting, Southern; D001973:Bromodeoxyuridine / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D000242:Cyclic AMP / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D015870:Gene Expression / Q000187:drug effects; D006160:Guanosine Triphosphate / Q000494:pharmacology; D006165:Guanylyl Imidodiphosphate / Q000494:pharmacology; D006801:Humans; D007097:Imines / Q000494:pharmacology; D007456:Iodine Isotopes / Q000493:pharmacokinetics; D008223:Lymphoma; D010446:Peptide Fragments / Q000494:pharmacology; D010451:Peptide PHI / Q000494:pharmacology*; D037342:Pertussis Toxin / Q000494:pharmacology; D011485:Protein Binding / Q000187:drug effects; D012333:RNA, Messenger / Q000096:biosynthesis; D011869:Radioligand Assay / Q000379:methods; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D051236:Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide; D018005:Receptors, Vasoactive Intestinal Peptide / Q000235:genetics / Q000378:metabolism*; D051239:Receptors, Vasoactive Intestinal Peptide, Type II; D051238:Receptors, Vasoactive Intestinal Polypeptide, Type I; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013997:Time Factors; D014660:Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors / Q000494:pharmacology*
chemical_list: D000067956:Adenylyl Cyclase Inhibitors; D007097:Imines; D007456:Iodine Isotopes; D010446:Peptide Fragments; D010451:Peptide PHI; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D051236:Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide; D018005:Receptors, Vasoactive Intestinal Peptide; D051239:Receptors, Vasoactive Intestinal Peptide, Type II; D051238:Receptors, Vasoactive Intestinal Polypeptide, Type I; C495506:VIPR1 protein, human; C017759:9-(tetrahydro-2-furyl)-adenine; D006165:Guanylyl Imidodiphosphate; D014660:Vasoactive Intestinal Peptide; C047945:vasoactive intestinal peptide (10-28); C014925:RMI 12330A; D006160:Guanosine Triphosphate; D000242:Cyclic AMP; D037342:Pertussis Toxin; D001973:Bromodeoxyuridine; D000225:Adenine