Regulation of [Ca2+]i rise activated by doxepin-sensitive H1-histamine receptors in jurkat cells,cloned human T lymphocytes |
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| Affiliation: | 1. Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo 060, Japan [Tel: 81-11-706-3246, Fax: 81-11-706-4987];2. Department of Neurosciences Research Institute for Oriental Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan;1. Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, TN, USA;2. Chemical and Physical Biology Program, Vanderbilt University, Nashville, TN, USA;3. Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA;4. Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, USA;5. School of Health Sciences, Purdue University, West Lafayette, IN, USA;6. Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, USA;7. Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, USA;8. Department of Physics and Astronomy, Vanderbilt University, Nashville, TN, USA;9. Vanderbilt Institute for Integrative Biosystems Research and Education, Vanderbilt University, Nashville, TN, USA;1. Civil Engineering Department, College of Engineering, Salahaddin University-Erbil, Kurdistan, Iraq;2. Civil Engineering Department, College of Engineering, Tishk International University-Erbil, Erbil, Kurdistan Region, Iraq;3. Civil Engineering Department, College of Engineering, University of Sulaimani, Kurdistan, Iraq;4. The American University of Iraq, Sulaimani (AUIS), Sulaimani, Kurdistan Region. Iraq;5. Department of Highway and Bridge Engineering, Technical Engineering College, Erbil Polytechnic University, Erbil 44001, Iraq;6. Department of Civil Engineering, College of Engineering, University of Duhok, Duhok, Kurdistan-Region, Iraq;7. Computational Mechanics Laboratory, School of Pedagogical and Technological Education, Athens, Greece;1. Department of Obstetrics and Gynecology, Ataturk Duzce State Hospital, Duzce, Turkey;2. Department of Obstetrics and Gynecology, Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Turkey;3. Department of Obstetrics and Gynecology, Fatih Sultan Mehmet Training and Research Hospital, Istanbul, Turkey;1. JET-EFDA, Culham Science Centre, Abingdon OX14 3DB, UK;2. Laboratory for Plasma Physics, ERM/KMS, TEC Partner, 1000 Brussels, Belgium;3. CEA, IRFM, F-13108 St-Paul-Lez-Durance, France;4. Forschungszentrum Jülich, Institut für Energie- und Klimaforschung Plasmaphysik, 52425 Jülich, Germany;5. Max-Planck Institut für Plasmaphysik, 85748 Garching, Germany;6. Jožef Stefan Institute, 1000 Ljubljana, Slovenia;7. IST, Instituto de Plasmas e Fusão Nuclear, 1049-001 Lisboa, Portugal |
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| Abstract: | To clarify the presence of histamine receptor and its transmembrane mechanism in human T lymphocytes, we investigated the effects of agonists or antagonists of histamine receptor subtypes and bacterial toxins on intracellular concentration of Ca2+ [Ca2+]i, [3H]pyrilamine binding and c-fos mRNA expression in Jurkat cells, cloned human T lymphocytes. H1-agonists (histamine and 2-methyl-histamine) caused a transient rise of [Ca2+], and H1-antagonists (pyrilamine and doxepin) inhibited the histamine-induced [Ca2+]i rise more potently than the H2-antagonist (cimetidine) on the H3-antagonist (impromidine). Binding parameters of [3H]pyrilamine binding were Kd=5.53 nM and Bmax = 2,647 sites/ cell. Pretreatment with B.pertussis, V. cholera. orC. botulinum toxin did not influence histamine-induced [Ca2+]i rise. Western Blot analysis using antibodies against subunits of GTP-binding proteins indicated that Gq/G11 richly existed in Jurkat cells. Histamine induced mRNA expression of an immediate early gene c-fos. Pretreatment with a protein kinase C activator, phorbol 12-myristate 13-acetate, caused almost complete inhibition of histamine-induced [Ca2+]i rise, but did not do so by activators of cAMP- and cGMP-dependent protein kinases. |
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