ACELL November 46/5
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چکیده
Prinz, Christian, Robert Zanner, Markus Gerhard, Sabine Mahr, Nina Neumayer, Barbara Höhne-Zell, and Manfred Gratzl. The mechanism of histamine secretion from gastric enterochromaffin-like cells. Am. J. Physiol. 277 (Cell Physiol. 46): C845–C855, 1999.— Enterochromaffin-like (ECL) cells play a pivotal role in the peripheral regulation of gastric acid secretion as they respond to the functionally important gastrointestinal hormones gastrin and somatostatin and neural mediators such as pituitary adenylate cyclase-activating peptide and galanin. Gastrin is the key stimulus of histamine release from ECL cells in vivo and in vitro. Voltage-gated K1 and Ca21 channels have been detected on isolated ECL cells. Exocytosis of histamine following gastrin stimulation and Ca21 entry across the plasma membrane is catalyzed by synaptobrevin and synaptosomal-associated protein of 25 kDa, both characterized as a soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein. Histamine release occurs from different cellular pools: preexisting vacuolar histamine immediately released by Ca21 entry or newly synthesized histamine following induction of histidine decarboxylase (HDC) by gastrin stimulation. Histamine is synthesized by cytoplasmic HDC and accumulated in secretory vesicles by protonhistamine countertransport via the vesicular monoamine transporter subtype 2 (VMAT-2). The promoter region of HDC contains Ca21-, cAMP-, and protein kinase C-responsive elements. The gene promoter for VMAT-2, however, lacks TATA boxes but contains regulatory elements for the hormones glucagon and somatostatin. Histamine secretion from ECL cells is thereby under a complex regulation of hormonal signals and can be targeted at several steps during the process of exocytosis.
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ACELL November 46/5
ESTHER TITOS,1 NAN CHIANG,2 CHARLES N. SERHAN,2 MARIO ROMANO,3 JOAN GAYA,4 GLORIA PUEYO,5 AND JOAN CLÀRIA1 1DNA Unit and 4Hormonal Laboratory, Institut d’Investigacions Biomèdiques August Pi i Sunyer, Hospital Clı́nic and 5Quı́mica Farmacéutica Bayer (Consumer Care Division), Barcelona 08036, Spain; 2Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Periop...
متن کاملACELL November 46/5
Carbajal, José M., and Richard C. Schaeffer, Jr. RhoA inactivation enhances endothelial barrier function. Am. J. Physiol. 277 (Cell Physiol. 46): C955–C964, 1999.—The modulation of endothelial barrier function is thought to be a function of contractile tension mediated by the cell cytoskeleton, which consists of actomyosin stress fibers (SF) linked to focal adhesions (FA). We tested this hypoth...
متن کاملACELL September 46/3
Zeiske, Wolfgang, Ilse Smets, Marcel Ameloot, Paul Steels, and Willy Van Driessche. Intracellular pH shifts in cultured kidney (A6) cells: effects on apical Na1 transport. Am. J. Physiol. 277 (Cell Physiol. 46): C469–C479, 1999.—We report, for the epithelial Na1 channel (ENaC) in A6 cells, the modulation by cell pH (pHc) of the transepithelial Na1 current (INa), the current through the individu...
متن کاملACELL November 46/5
Van Den Abbeele, Thierry, Jacques Teulon, and Patrice Tran Ba Huy. Two types of voltage-dependent potassium channels in outer hair cells from the guinea pig cochlea. Am. J. Physiol. 277 (Cell Physiol. 46): C913–C925, 1999.— Cell-attached and cell-free configurations of the patch-clamp technique were used to investigate the conductive properties and regulation of the major K1 channels in the bas...
متن کاملACELL October 46/4
NABENDU S. CHATTERJEE,1 CHANDIRA K. KUMAR,1 ALVARO ORTIZ,1 STANLEY A. RUBIN,2 AND HAMID M. SAID1 1Medical Research Service, Veterans Affairs Medical Center, Long Beach 90822, and Department of Medicine and Physiology/Biophysics, University of California School of Medicine, Irvine 92697; and 2Veterans Affairs West Los Angeles, Los Angeles 90073, and Department of Medicine, University of Californ...
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