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Histamine upregulates the expression of inducible nitric oxide synthase in human intimal smooth muscle cells via histamine H1 receptor and NF-kappaB signaling pathway.
Arterioscler Thromb Vasc Biol. 2007 Jul; 27(7):1556-61.AT

Abstract

OBJECTIVE

Histamine increases endothelial nitric oxide (NO) production as an endothelium-dependent vasodilator, which acts as a vasoconstrictor in atherosclerotic coronary arteries. To investigate the relation between histamine and NO production in intimal smooth muscle cells (SMCs), we studied the effect of histamine on inducible NO synthase (iNOS) expression in the SMCs.

METHODS AND RESULTS

In cultured human intimal SMCs, histamine increased NO production, iNOS expression, and NF-kappaB nuclear translocation, which were inhibited by histamine H1 blocker and NF-kappaB inhibitor. Luciferase assay using -8.3 kb upstream of human iNOS promoter region and electrophoretic mobility shift assay suggested that a NF-kappaB motif located at -3922 to -3914 would be necessary for histamine-inducible promoter activity. In addition, H1 blocker, NF-kappaB inhibitor, and dominant negative IkappaB alpha or IkappaB kinase beta downregulated the histamine-induced iNOS promoter activity. In the human aorta, histamine content was estimated to be 310+/-66 pmol/mg protein in the atherosclerotic intima, while that was to be 43+/-22 pmol/mg protein in the media (P<0.001).

CONCLUSIONS

Histamine stimulates intimal SMCs to increase iNOS expression via H1 receptors and NF-kappaB signaling pathway. Histamine could be one of NO-regulating factors, by inducing iNOS expression in intimal SMCs, and may be related to atherogenesis.

Authors+Show Affiliations

Department of Pathology and Cell Biology, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi, Kitakyushu 807-8555, Japan. aki@med.uoeh-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17478759

Citation

Tanimoto, Akihide, et al. "Histamine Upregulates the Expression of Inducible Nitric Oxide Synthase in Human Intimal Smooth Muscle Cells Via Histamine H1 Receptor and NF-kappaB Signaling Pathway." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 27, no. 7, 2007, pp. 1556-61.
Tanimoto A, Wang KY, Murata Y, et al. Histamine upregulates the expression of inducible nitric oxide synthase in human intimal smooth muscle cells via histamine H1 receptor and NF-kappaB signaling pathway. Arterioscler Thromb Vasc Biol. 2007;27(7):1556-61.
Tanimoto, A., Wang, K. Y., Murata, Y., Kimura, S., Nomaguchi, M., Nakata, S., Tsutsui, M., & Sasaguri, Y. (2007). Histamine upregulates the expression of inducible nitric oxide synthase in human intimal smooth muscle cells via histamine H1 receptor and NF-kappaB signaling pathway. Arteriosclerosis, Thrombosis, and Vascular Biology, 27(7), 1556-61.
Tanimoto A, et al. Histamine Upregulates the Expression of Inducible Nitric Oxide Synthase in Human Intimal Smooth Muscle Cells Via Histamine H1 Receptor and NF-kappaB Signaling Pathway. Arterioscler Thromb Vasc Biol. 2007;27(7):1556-61. PubMed PMID: 17478759.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Histamine upregulates the expression of inducible nitric oxide synthase in human intimal smooth muscle cells via histamine H1 receptor and NF-kappaB signaling pathway. AU - Tanimoto,Akihide, AU - Wang,Ke-Yong, AU - Murata,Yoshitaka, AU - Kimura,Satoshi, AU - Nomaguchi,Masako, AU - Nakata,Sei, AU - Tsutsui,Masato, AU - Sasaguri,Yasuyuki, Y1 - 2007/05/03/ PY - 2007/5/5/pubmed PY - 2007/7/10/medline PY - 2007/5/5/entrez SP - 1556 EP - 61 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 27 IS - 7 N2 - OBJECTIVE: Histamine increases endothelial nitric oxide (NO) production as an endothelium-dependent vasodilator, which acts as a vasoconstrictor in atherosclerotic coronary arteries. To investigate the relation between histamine and NO production in intimal smooth muscle cells (SMCs), we studied the effect of histamine on inducible NO synthase (iNOS) expression in the SMCs. METHODS AND RESULTS: In cultured human intimal SMCs, histamine increased NO production, iNOS expression, and NF-kappaB nuclear translocation, which were inhibited by histamine H1 blocker and NF-kappaB inhibitor. Luciferase assay using -8.3 kb upstream of human iNOS promoter region and electrophoretic mobility shift assay suggested that a NF-kappaB motif located at -3922 to -3914 would be necessary for histamine-inducible promoter activity. In addition, H1 blocker, NF-kappaB inhibitor, and dominant negative IkappaB alpha or IkappaB kinase beta downregulated the histamine-induced iNOS promoter activity. In the human aorta, histamine content was estimated to be 310+/-66 pmol/mg protein in the atherosclerotic intima, while that was to be 43+/-22 pmol/mg protein in the media (P<0.001). CONCLUSIONS: Histamine stimulates intimal SMCs to increase iNOS expression via H1 receptors and NF-kappaB signaling pathway. Histamine could be one of NO-regulating factors, by inducing iNOS expression in intimal SMCs, and may be related to atherogenesis. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/17478759/Histamine_upregulates_the_expression_of_inducible_nitric_oxide_synthase_in_human_intimal_smooth_muscle_cells_via_histamine_H1_receptor_and_NF_kappaB_signaling_pathway_ L2 - https://www.ahajournals.org/doi/10.1161/ATVBAHA.106.139089?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -