Histamine H2 receptor activates adenylate cyclase and PLC via separate GTP-dependent pathways

Wang, L.; Gantz, Ira; DelValle, John

doi:10.1152/ajpgi.1996.271.4.g613

Cited by 22 publications

(21 citation statements)

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“…This was confirmed in experiments with a cloned H 2 receptor in which the direct linkage of a single receptor to both adenylyl cyclase and PLC via separate GTP-dependent mechanisms was demonstrated (37,38). Several other reports also showed that a single type of receptor may be associated with more than one G protein and thus lead to multiple intracellular signaling systems, although the mechanism by which different factors may be involved in regulation of the plurality of receptor-mediated signaling remains unknown.…”

Section: Discussionmentioning

confidence: 72%

Inhibition of H2 Histamine Receptor-Mediated Cation Channel Opening by Protein Kinase C in Human Promyelocytic Cells

Suh

Lee

Jun

et al. 2001

The Journal of Immunology

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Histamine, through H2 receptors, triggers a prominent rise in intracellular free Ca2+ concentration ([Ca2+]i) in addition to an elevation of cAMP level in HL-60 promyelocytes. Here we show that the histamine-induced [Ca2+]i rise was due to influx of Ca2+ from the extracellular space, probably through nonselective cation channels, as incubation of the cells with SKF 96365 abolished the histamine-induced [Ca2+]i rise, Na+ influx, and membrane depolarization. The Ca2+ influx was specifically inhibited by pretreatment of the cells with PMA or extracellular ATP with 50% inhibitory concentrations of 0.12 ± 0.03 nM and 185 ± 17 μM, respectively. Western blot analysis of protein kinase C (PKC) isoforms revealed that PMA (≤1 nM) and ATP (300 μM) caused selective translocation of PKC-δ to the particulate/membrane fraction. Costimulation of the cells with histamine and SKF 96365 partially reduced histamine-induced granulocytic differentiation, which was evaluated by looking at the extent of fMet-Leu-Phe-induced [Ca2+]i rise and superoxide generation. In conclusion, nonselective cation channels are opened by stimulation of the H2 receptor, and the channels are at least in part involved in the induction of histamine-mediated differentiation processes. Both effects of histamine were selectively inhibited probably by the δ isoform of PKC in HL-60 cells.

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Section: Discussionmentioning

confidence: 72%

Inhibition of H2 Histamine Receptor-Mediated Cation Channel Opening by Protein Kinase C in Human Promyelocytic Cells

Suh

Lee

Jun

et al. 2001

The Journal of Immunology

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“…Histamine mediated activation of its receptor leads to signaling through both adenylate cyclase (AC) and phosphoinositide (PI)/protein kinase C (PKC) second messenger systems (2,5). This observation has been made in both primary systems such as the parietal cell (6 -8) as well as in transfected cell models (9,10). The importance of this receptor in regulating multiple physiological events lends relevance to elucidating the pathways involved in post-receptor signaling.…”

mentioning

confidence: 94%

Histamine H2 Receptor Mediated Dual Signaling: Mapping of Structural Requirements Using β2 Adrenergic Chimeric Receptors

Wang

Gantz

Butler

et al. 2000

Biochemical and Biophysical Research Communications

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“…Interestingly, antihistamine drugs were neuroprotective only when both H 1 and H 2 histamine receptors were blocked. H 2 receptors are linked to both adenylate cyclase and phospholipase C in pathways that lead to calcium mobilization (27)(28)(29). The phospholipase C pathway is also used by H 1 receptors.…”

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confidence: 99%

Deleterious Effects of IL-9–Activated Mast Cells and Neuroprotection by Antihistamine Drugs in the Developing Mouse Brain

et al. 2001

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Elevated mean IL-9 serum levels have been observed in human neonates who will later develop cerebral palsy. In earlier studies, using a newborn mouse model of excitotoxic lesions mimicking those described in human cerebral palsy, we found that IL-9 pretreatment exacerbated brain damage produced by intracerebral injections of the glutamatergic analog ibotenate. Among its different cell targets, the Th2 cytokine IL-9 is a mast cell growth and differentiation factor that can cause mast cells to release various substances including histamine. In the present study, we sought to determine whether the deleterious effects of IL-9 in our mouse model were mediated by mast cells through histamine release. All mouse pups were pretreated with intraperitoneal injections of IL-9 or saline between postnatal days (P) P1 and P5. Immunohistochemistry for murine mast cell protease-1 performed on P5 showed an increased density of labeled cells in the neopallium of IL-9 -treated Swiss pups as compared with controls. Western blot analysis confirmed the increased murine mast cell protease-1 brain content of IL-9 -treated Swiss mice. IL-9 pretreatment had no significant effect on ibotenateinduced excitotoxic brain lesions in mast cell-deficient P5 pups (WBB6F1/J kit W/W-v ), whereas IL-9 exacerbated these lesions in the control littermates with normal mast cell populations. Finally, cromoglycate or antihistamine drugs significantly reduced ibotenate-induced brain lesions in IL-9 -treated Swiss pups. Taken together, these data suggest that recruitment of cerebral mast cells with histamine release may contribute to the exacerbation of neonatal excitotoxic brain lesions produced by IL-9. Neuroprotective strategies targeting mast cells may be useful in some neonates at risk for cerebral palsy. (1-7). Recent hypotheses have implicated multiple preconceptional and prenatal factors, such as hypoxiaperfusion failure, genetic factors, growth factor deficiency, and excess production of cytokines. In a striking retrospective study, mean levels of perinatal circulating cytokines-including IL-1␤, IL-6, IL-8, IL-9, and TNF-␣-were higher in patients with subsequent occurrence of cerebral palsy than in control subjects (8).In that study, although the numbers of included patients were limited, levels of proinflammatory cytokines (IL-1-␤, IL-6, IL-8, and TNF-␣) were associated with one another, but no correlation was detected between IL-9 levels and the levels of the other cytokines tested. Although further studies will be necessary to confirm this initial observation, these data could suggest the existence of a subpopulation of cerebral palsy patients characterized by increased levels of circulating IL-9 at birth. A better understanding of the mechanisms bridging IL-9 blood level elevation and brain damage might open up new therapeutic possibilities for preventing cerebral palsy in infants with high circulating IL-9 levels.Intracerebral injection of ibotenate, a glutamate analog, to newborn mice produces histologic lesions mimicking the brain lesions f...

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Histamine H2 receptor activates adenylate cyclase and PLC via separate GTP-dependent pathways

Cited by 22 publications

References 0 publications

Inhibition of H2 Histamine Receptor-Mediated Cation Channel Opening by Protein Kinase C in Human Promyelocytic Cells

Inhibition of H2 Histamine Receptor-Mediated Cation Channel Opening by Protein Kinase C in Human Promyelocytic Cells

Histamine H2 Receptor Mediated Dual Signaling: Mapping of Structural Requirements Using β2 Adrenergic Chimeric Receptors

Deleterious Effects of IL-9–Activated Mast Cells and Neuroprotection by Antihistamine Drugs in the Developing Mouse Brain

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