12-O-Tetradecanoylphorbol-13-acetate stimulates the transcription of the histidine decarboxylase gene

Yatsunami, Kimio; Nakagawa, Satoshi; Ohgo, Makoto; Yamamoto, Jun; Ichikawa, Atsushi

doi:10.1007/bf01996445

Cited by 4 publications

(4 citation statements)

References 8 publications

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“…Recent studies [7,8] have confirmed much earlier observations [9] that histamine synthesis is inducible in a variety of tissues. Induction can be by a wide range of stimuli, examples include gastrin in the gastric mucosa, phorbol esters in the skin and endotoxin shock in the lung [7][8][9][10].…”

Section: Discussionsupporting

confidence: 69%

“…Induction can be by a wide range of stimuli, examples include gastrin in the gastric mucosa, phorbol esters in the skin and endotoxin shock in the lung [7][8][9][10]. In our hands allergen exposure induced HFC but, although this induction could be increased by an H 3 receptor antagonist, the agonist c~ methyl histamine did not affect it significantly possibly due to the fact that mast cell derived histamine was already maximally stimulating the H 3 receptor during exposure to allergen.…”

Section: Discussionmentioning

confidence: 99%

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Histamine forming capacity (HFC) and its modulation by H3 receptor ligands in a model of bronchial hyper-responsiveness

1996

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The histamine forming capacity (HFC) of acutely challenged airways from sensitised guinea pigs was investigated. After exposure to nebulised bovine serum albumin (BSA) or normal saline, animals were sacrificed, the pulmonary HFC determined and concurrent in vitro histamine log concentration response curves were constructed for parenchymal strips and tracheal muscle, the latter was field stimulated to record neurogenic responses. Exposure to BSA increased the HFC above controls for 24 hours (p < 0.001) and log concentration response curves for the parenchymal strips were shifted slightly to the left with an increased maximum response. This change appeared 3 hours after exposure and remained elevated at 24 hours. Similar changes did not occur with the trachea. Pre-treatment with thioperamide augmented (p < 0.02) HFC and this increase was inhibited by alpha-methylhistamine (p < 0.05). A possible relationship may exist between increased responsiveness of lower airways to exogenous histamine and a raised endogenous formation, regulated by the H3 receptor.

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Histamine forming capacity (HFC) and its modulation by H3 receptor ligands in a model of bronchial hyper-responsiveness

1996

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“…Previous studies suggested that TPA treatment led to increased HDC transcription in KU-812-F cells (12) and increased binding to the TPA response element (TRE) (TGACTCA) of a nuclear factor (presumably AP1) in mouse mastocytoma P-815 cells (39), but the absence of an obvious TRE site in the human HDC 5Ј-flanking region raised the possibility that the HDC promoter may respond to phorbol esters through other mechanisms (36). The most common phorbol ester response element or TRE is the binding site for AP1, but the TRE is only one of several cis-acting elements that mediate induction responses to TPA and other activators of PKC.…”

Section: Creation Of Human Hdc-luciferase Constructs and Analysis Of mentioning

confidence: 99%

The Human Histidine Decarboxylase Promoter Is Regulated by Gastrin and Phorbol 12-Myristate 13-Acetate through a Downstream -Acting Element

Zhang

Höcker

Koh

et al. 1996

Journal of Biological Chemistry

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OligonucleotidesSequences (5Ј 3 3Ј) Ϫ125 to Ϫ108, sense CCCAAGCTTGGGCCTGGCTCTCTTGACCAG Ϫ73 to Ϫ60, sense CCCAAGCTTGGGAAAGAAAGGGTGGAAT Ϫ59 to Ϫ42, sense CCCAAGCTTGGGAATTAATTAAACCTGG Ϫ47 to Ϫ30, sense CCCAAGCTTGGGACCTGGAGGAAGGGACTT ϩ126 to ϩ109, antisense CCGCTCGAGCGGCTGGCTCCTTCTCACAGA ϩ36 to ϩ19, antisense CCGCTCGAGCGGCCCTGGCAGCCAGTGTGG ϩ20 to ϩ3, antisense CCGCTCGAGCGGGCCCTTTATTTAAAGG ϩ14 to Ϫ4, antisense CCGCTCGAGCGGTTTATTTAAAGGGTTCTT ϩ3 to Ϫ15, antisense CCGCTCGAGCGGTTCTTTCTTTGACCTT Regulation of Human HDC Gene

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“…Many investigators demonstrated that HDC regulates the level of histamine in tissues or cells, and that modulation of HDC activity under various conditions markedly affects the level of the amine (Schneider et al, 1987;Mamune-Sato et al, 1990;Yatsunami et al, 1993). It is thus of great importance to clarify the mechanism underlying regulation of the HDC activity.…”

mentioning

confidence: 99%

Comparative Studies of Human Recombinant 74- and 54-kDa L-Histidine Decarboxylases

Yatsunami

Tsuchikawa

Kamada

et al. 1995

Journal of Biological Chemistry

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We have expressed and characterized human recombinant 74-kDa (rHDC74) and 54-kDa (rHDC54) L-histidine decarboxylases (HDCs) in Sf9 cells. By immunoblot analysis, rHDC74 and rHDC54 were shown to be localized predominantly in the particulate and soluble fractions, respectively. rHDC74 exhibited histamine-synthesizing activity equivalent to that of rHDC54. The existence of 74-and 54-kDa HDCs was also confirmed in the particulate and supernatant fractions of the cell lysate, respectively, from the human basophilic leukemia cell line KU-812-F. The ratio of HDC activity to immunoreactivity was similar for the two forms of the enzyme. The specific activity of purified rHDC54 (1.12 mol/mg/min) was comparable to those of HDCs from other mammalian tissues or cells. The purified rHDC54 was eluted as a monomer form from a Superdex-200 column; the molecular mass of the enzyme was approximately 54 kDa on SDS-polyacrylamide gel electrophoresis without 2-mercaptoethanol. The HDC activity of rHDC54 significantly decreased on dialysis against buffer without pyridoxal 5-phosphate; addition of pyridoxal 5-phosphate to the dialysate readily increased in the enzyme activity to the original activity. Taken together, these results suggest that human HDC functions as both 74-and 54-kDa forms having equivalent HDC activity, which are localized in the particulate and soluble fractions, respectively, and that the latter form exhibits its activity as a monomer form.

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12-O-Tetradecanoylphorbol-13-acetate stimulates the transcription of the histidine decarboxylase gene

Cited by 4 publications

References 8 publications

Histamine forming capacity (HFC) and its modulation by H3 receptor ligands in a model of bronchial hyper-responsiveness

Histamine forming capacity (HFC) and its modulation by H3 receptor ligands in a model of bronchial hyper-responsiveness

The Human Histidine Decarboxylase Promoter Is Regulated by Gastrin and Phorbol 12-Myristate 13-Acetate through a Downstream -Acting Element

Comparative Studies of Human Recombinant 74- and 54-kDa L-Histidine Decarboxylases

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