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Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells

  • Authors:
    • Yusuke Nagashima
    • Koichiro Kako
    • Jun-Dal Kim
    • Akiyoshi Fukamizu
  • View Affiliations / Copyright

    Affiliations: Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan, Faculty of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan, Life Science Center of Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan
    Copyright: © Nagashima et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
  • Pages: 944-948
    |
    Published online on: August 27, 2012
       https://doi.org/10.3892/mmr.2012.1049
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Abstract

Histamine (HA), a mediator of inflammation, type I allergic responses and neurotransmission, is synthesized from L-histidine, the reaction of which is catalyzed by histidine decarboxylase (HDC). HDC has been reported to be induced by various stimuli, not only in mast cells and basophils, but also in T lymphocytes and macrophages. Although its mRNA has been shown to be increased in Jurkat cells when treated with phorbol 12-myristate 13-acetate (TPA), little is known concerning the induced production of HA by HDC. The present study quantified the trace amounts of intracellular HA using ultra-high liquid chromatography in combination with the 6-aminoquinoline carbamate-derivatization technique. To test whether the cellular level of HA is elevated by the induction of HDC in Jurkat cells treated with TPA, the peak corresponding to authentic HA in the cell lysate was fractioned and its molecular weight determined by matrix-assisted laser desorption/ionization quadrupole ion trap time-of-flight mass spectrometry. The results of this study show that the HA level is increased by the induction of HDC expression by TPA in Jurkat cells. Therefore, this method is useful in elucidating the physiological significance of HA production.
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Copy and paste a formatted citation
Spandidos Publications style
Nagashima Y, Kako K, Kim J and Fukamizu A: Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells. Mol Med Rep 6: 944-948, 2012.
APA
Nagashima, Y., Kako, K., Kim, J., & Fukamizu, A. (2012). Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells. Molecular Medicine Reports, 6, 944-948. https://doi.org/10.3892/mmr.2012.1049
MLA
Nagashima, Y., Kako, K., Kim, J., Fukamizu, A."Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells". Molecular Medicine Reports 6.5 (2012): 944-948.
Chicago
Nagashima, Y., Kako, K., Kim, J., Fukamizu, A."Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells". Molecular Medicine Reports 6, no. 5 (2012): 944-948. https://doi.org/10.3892/mmr.2012.1049
Copy and paste a formatted citation
x
Spandidos Publications style
Nagashima Y, Kako K, Kim J and Fukamizu A: Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells. Mol Med Rep 6: 944-948, 2012.
APA
Nagashima, Y., Kako, K., Kim, J., & Fukamizu, A. (2012). Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells. Molecular Medicine Reports, 6, 944-948. https://doi.org/10.3892/mmr.2012.1049
MLA
Nagashima, Y., Kako, K., Kim, J., Fukamizu, A."Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells". Molecular Medicine Reports 6.5 (2012): 944-948.
Chicago
Nagashima, Y., Kako, K., Kim, J., Fukamizu, A."Enhanced histamine production through the induction of histidine decarboxylase expression by phorbol ester in Jurkat cells". Molecular Medicine Reports 6, no. 5 (2012): 944-948. https://doi.org/10.3892/mmr.2012.1049
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