Intracellular histamine and liver regeneration: High affinity binding of histamine to chromatin, low affinity binding to matrix, and depletion of a nuclear storage pool following partial hepatectomy

Brandes, Lorne J.; Bogdanovic, R.Patricia; Tong, Jiangang; Davie, James R.; LaBella, Frank S.

doi:10.1016/0006-291x(92)90666-9

Cited by 28 publications

(17 citation statements)

References 20 publications

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“…HDC has been shown to be activated in tissues undergoing rapid growth (Kahlson et al, 1963), and histamine has been shown to promote cell proliferation of human carcinoma and melanoma cells under serum free conditions (Tilly et al, 1990). Intracellular histamine is involved in platelet aggregation (Saxena et al, 1989), and intracellular binding site mechanisms have been proposed for histamine in regenerating tissues, particularly liver (Brandes et al, 1992). A combination of pyridoxine deficient diet and semicarbazide, an inhibitor of several enzymes including HDC during pregnancy, arrests the fetal growth and leads to its death (Kahlson and Rosengren, 1959).…”

Section: Discussionmentioning

confidence: 99%

In situ detection of H1-receptor mRNA and absence of apoptosis in the transient histamine system of the embryonic rat brain

et al. 1998

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In the developing brain, histamine is one of the first neurotransmitters to appear. The concentration of histamine in the prenatal brain is fivefold that of adult levels. During the prenatal development a large transiently histamine-immunoreactive cell population distinct from the adult histaminergic system can be found within a subpopulation of the developing serotonergic raphe nuclei neurons. Also histamine-immunoreactive nerve fibers are widely distributed already during the prenatal development extending to the diencephalon, the thalamus, the cortex, and the spinal cord. Large numbers of histamine-containing mast cells also migrate into the brain during the late prenatal life. The wide distribution and high prenatal concentrations imply important functions for the histaminergic system during intrauterine development. However, little is known about the actual functions of histamine during development, and which of the histamine receptors are present in the prenatal rat brain is currently unknown. In the present study, we used in situ hybridization to study the distribution of H1-receptor (H1R) mRNA in the embryonic rat brain and spinal cord. H1R mRNA could be detected in rat brain and in spinal cord on embryonic day (E) 14, and the expression pattern seemed to partially localize in areas containing histamine-immunoreactive nerve fibers through E14-E20. H1R mRNA was also detected by reverse transcriptase polymerase chain reaction from embryonic brain samples and by Northern hybridization. The possible involvement of apoptosis in the disappearance of the developing transiently histaminergic system was studied by using apoptosis detection based on the terminal dUTP nick end labeling (TUNEL) technique and with c-Fos immunostaining. Although histamine immunoreactivity disappears dramatically from the developing raphe nuclei after E18, only occasional apoptotic nuclei could be seen in the histamine-immunoreactive cell bodies. The presence of H1R mRNA during the embryonic development renders it possible that histamine could exert an H1R-specific function at the time of the embryonic histamine peak.

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Section: Discussionmentioning

confidence: 99%

In situ detection of H1-receptor mRNA and absence of apoptosis in the transient histamine system of the embryonic rat brain

et al. 1998

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“…Hie, has been presented recently. This receptor is microsomal and ap pears to be associated with the anticstrogen binding site, and may bind histamine released from intracellular stores and thereby effect cell proliferation [39,52], The Hie site has been reported to mediate proliferation of numerous cell types, including several tumors [53] and tumor cell lines in culture [54], Questions have however been raised in regard to the existence of an Hjc in histamine-produc ing cells. Since the vesicles accumulate histamine presum ably via an H+ antiportcr mechanism, there is presumably always a finite concentration of histamine on the exterior of the vacuole.…”

Section: Discussionmentioning

confidence: 99%

Evidence for a Regulatory Role for Histamine in Gastric Enterochromaffin-Like Cell Proliferation Induced by Hypergastrinemia

Modlin

Zhu²,

Tang³

et al. 1996

Digestion

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Background/Aims: Hypergastrinemia, induced by sustained suppression of gastric acid secretion, is associated with gastric enterochromaffin-like (ECL) cell hyperplasia and carcinoid tumor formation. We examined the effect of a selective Hi-histamine antagonist, terfenadine, on gastric mucosal cell proliferation to determine whether histamine might modulate ECL cell generation. Methods: The rodent mastomys received the H₂-antagonist loxtidine (2 g/l drinking water) alone or in combination with terfenadine (0.5 g/l or 35 mg/l drinking water) for 120 days. Controls received water or terfenadine alone. Serum gastrin levels and tissue histamine content were assayed by radioimmu-noassays, and tissue chromogranin levels determined (Western blot analysis). In vivo cell proliferation was measured by bromodeoxyuridine (BrdU, 200 mg/kg/day, 3 days) incorporation. Gastric mucosal thickness was determined, ECL cell number was assessed, and the percentage of proliferating ECL cells quantitated. To evaluate the direct action on ECL cells we then studied the effect of terfenadine on histamine secretion and DNA synthesis (BrdU uptake) in an isolated preparation (∼ 90% pure) of ECL cells. Results: Loxtidine increased serum gastrin levels, mucosal thickness, tissue chromogranin levels, tissue histamine content, BrdU incorporation, ECL cell number, and proliferating ECL cells (all parameters p < 0.05). Terfenadine alone, irrespective of dosage, had no significant effect. The high dose in combination with loxtidine significantly inhibited the increase in tissue chromogranin levels, tissue histamine content, ECL cell number and proliferating ECL cells (p < 0.05), but did not alter other parameters, compared to loxtidine alone. The low dose did not alter the loxtidine-induced changes. In pure isolated ECL cells, terfenadine did not alter histamine secretion either alone or in combination with gastrin (10 nM). DNA synthesis was significantly inhibited by terfenadine (IC₅₀ 10^-10M). Conclusions: Terfenadine specifically inhibited the effect of loxtidine-induced ECL cell proliferation in vivo and significantly inhibited ECL cell DNA synthesis in vitro. We postulate that histamine, through an H₁ receptor, positively modulates gastric ECL cell proliferation.

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“…A tamoxifen derivative N,N-diethyl-2-[4-(phenylmethyl) phenoxy]-ethanamine HCl (DPPE), with a still not fully elucidated molecular mechanism, disturbs some effects of histamine effects [8]. In platelet aggregation [2] and cell proliferation DPPE inhibits the effects of histamine.…”

Section: Discussionmentioning

confidence: 99%

“…The importance of intracellular histamine has been demonstrated in wound healing [4], embryonic development [5], hematopoiesis [6,7], regeneration of liver [8] and in several tumors [9]. Endogenously produced histamine acting in an autocrine or intracrine way has been implicated as a mediator of cellular division and/or differentiation in both normal and neoplastic tissues [10 -12].…”

Section: Introductionmentioning

confidence: 99%

Increased histidine decarboxylase expression during in vitro monocyte maturation; a possible role of endogenously synthesised histamine in monocyte/macrophage differentiation

et al. 2001

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Intracellular histamine and liver regeneration: High affinity binding of histamine to chromatin, low affinity binding to matrix, and depletion of a nuclear storage pool following partial hepatectomy

Cited by 28 publications

References 20 publications

In situ detection of H1-receptor mRNA and absence of apoptosis in the transient histamine system of the embryonic rat brain

In situ detection of H1-receptor mRNA and absence of apoptosis in the transient histamine system of the embryonic rat brain

Evidence for a Regulatory Role for Histamine in Gastric Enterochromaffin-Like Cell Proliferation Induced by Hypergastrinemia

Increased histidine decarboxylase expression during in vitro monocyte maturation; a possible role of endogenously synthesised histamine in monocyte/macrophage differentiation

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