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Molecular Pharmacology

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Research ArticleArticle

Histamine Induces Nuclear Factor of Activated T Cell-Mediated Transcription and Cyclosporin A-Sensitive Interleukin-8 mRNA Expression in Human Umbilical Vein Endothelial Cells

Valerie Boss, Xiaofei Wang, Lacie F. Koppelman, Kaiming Xu and T. J. Murphy
Molecular Pharmacology August 1998, 54 (2) 264-272; DOI: https://doi.org/10.1124/mol.54.2.264
Valerie Boss
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Xiaofei Wang
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Lacie F. Koppelman
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Kaiming Xu
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T. J. Murphy
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Abstract

The nuclear factor of activated T cells (NFAT) mediates a cyclosporin A (CsA)- and FK506-suppressible transcriptional program in lymphocytes after antigen-stimulated phospholipase C activation. Nonlymphoid cells also express NFAT isoforms, raising the possibility that these isoforms can be regulated by other extracellular stimuli. This study sought to determine whether histamine can trigger NFAT-mediated transcription in human umbilical vein endothelial cells (HUVEC), using a retrovirus-based luciferase reporter driven by a well characterized, NFAT-specific enhancer. Luciferase levels are induced up to 60-fold over basal levels after costimulation of HUVEC with Ca2+-mobilizing drugs and a phorbol ester, a response that is 20-fold greater than that observed when HUVEC are stimulated with either drug alone. These synergistic responses are inhibited in cells treated with CsA. CsA and FK506 also inhibit the luciferase response to histamine, indicating that histamine can induce NFAT-mediated transcription in HUVEC. To identify candidate genes in HUVEC that might be regulated by NFAT, the expression of several chemokine mRNAs was measured after histamine treatment. Of the mRNAs tested, only those encoding monocyte chemotactic protein-1 (∼2-fold over basal) and interleukin-8 (∼6-fold over basal) are induced by histamine; both of these responses are suppressed by CsA and FK506. The H1histamine receptor antagonist chlorpheniramine, but not the H2 receptor antagonist ranitidine, blocks the effects of histamine in this preparation. These data provide the first evidence for a physiological inducer of NFAT-mediated transcription in endothelial cells and support the hypothesis that NFAT participates in H1 histamine receptor-induced interleukin-8 gene expression.

Footnotes

    • Received January 12, 1998.
    • Accepted May 7, 1998.
  • Send reprint requests to: Dr. T. J. Murphy, Department of Pharmacology, 5031 O. W. Rollins Research Building, Emory University School of Medicine, Atlanta, GA 30322. E-mail:tmurphy{at}pharm.emory.edu

  • This work was supported by National Institutes of Health Grants HL52810, NS32706, and AR42687. T.J.M. is an Established Investigator of the American Heart Association. An abstract of this work was presented at the Experimental Biology Meeting 1998 (San Francisco, CA).

  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 54 (2)
Molecular Pharmacology
Vol. 54, Issue 2
1 Aug 1998
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Research ArticleArticle

Histamine Induces Nuclear Factor of Activated T Cell-Mediated Transcription and Cyclosporin A-Sensitive Interleukin-8 mRNA Expression in Human Umbilical Vein Endothelial Cells

Valerie Boss, Xiaofei Wang, Lacie F. Koppelman, Kaiming Xu and T. J. Murphy
Molecular Pharmacology August 1, 1998, 54 (2) 264-272; DOI: https://doi.org/10.1124/mol.54.2.264

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Research ArticleArticle

Histamine Induces Nuclear Factor of Activated T Cell-Mediated Transcription and Cyclosporin A-Sensitive Interleukin-8 mRNA Expression in Human Umbilical Vein Endothelial Cells

Valerie Boss, Xiaofei Wang, Lacie F. Koppelman, Kaiming Xu and T. J. Murphy
Molecular Pharmacology August 1, 1998, 54 (2) 264-272; DOI: https://doi.org/10.1124/mol.54.2.264
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