Oestradiol enhances in vitro the histamine release induced by embryonic histamine-releasing factor (EHRF) from uterine mast cells

Cocchiara, Roberta; Albeggiani, Giuseppe; Trapani, Giovanna Di; Azzolina, Antonina; Lampiasi, Nadia; Rizzo, F.; Diotallevi, Lidia; Gianaroli, Luca; Geraci, Domenico

doi:10.1093/oxfordjournals.humrep.a137790

Cited by 46 publications

(39 citation statements)

References 2 publications

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“…during the period propitious for embryo implantation [28], The current finding that RLX lacks the capacity to mediate de novo angiogenesis in the mesen tery implies that this hormone per se does not promote abdominal pregnancies which require de novo angiogene sis. It is moreover known that a factor in blastocyts induces mast-cell secretion at implantation [29,30] and that RLX is able to inhibit mast-cell secretion intraabdominally [31]. The physiologic surge of RLX in the peritoneal fluid should thus suppress mast-cell secretion in cases of intra-abdominal blastocyst implantation.…”

Section: Discussionmentioning

confidence: 99%

Relaxin, a Potent Microcirculatory Effector, Is Not Angiogenic

Norrby

Bani

Bigazzi³

et al. 1996

Int J Microcirc

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The ability of relaxin (RLX), which is a potent microcirculatory effector in many species including the rat, to induce de novo angiogenesis in vascularized mammalian tissue was tested using the rat mesenteric-window angiogenesis assay. RLX was administered intraperitoneally on days 1-5 at doses of 0.33, 3.3 and 33 nM. Controls received the vehicle by the same route. Groups of animals were sacrificed at the end of the 1st, 2nd and 3rd weeks. Using computer-aided microscopic morphometry including image analysis, the response was quantified by sensitive, technically independent, highly reproducible methods in terms of the vascularized area (VA), a measure of microvascular spatial extension, and the microvascular length (MVL), a measure of microvascular density. The total MVL was computed from VA × MVL. The results obtained show that RLX did not cause significant changes in any of the variables tested, regardless of dose and observation time. These findings indicate that RLX is apparently unable to mediate significant de novo angiogenesis in the system used in contrast to previously tested angiogens such as basic fibroblast growth factor, vascular endothelial growth factor, isoform 165, and tumor necrosis factor-α. In previous studies, RLX has been shown to exert antitumor activity on breast cancer cells in vitro. In the search for a possible role for RLX as an anticancer agent in vivo, it is important to know that this peptide is not angiogenic, since de novo angiogenesis is known to be a prerequisite for tumor growth and metastatic spread.

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Section: Discussionmentioning

confidence: 99%

Relaxin, a Potent Microcirculatory Effector, Is Not Angiogenic

Norrby

Bani

Bigazzi³

et al. 1996

Int J Microcirc

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“…Super-physiological concentrations of estradiol (E 2 , 1-10 μM) has been shown to induce (Spanos et al, 1996;Vliagoftis et al, 1992) or inhibit (Harnish et al, 2004) mast cell degranulation. Further, preincubating basophils or mast cells with physiological concentrations of E 2 has been shown to increase the subsequent histamine release induced by cross-linking surface-bound IgE with antibodies (Cocchiara et al, 1990;Cocchiara et al, 1992). The effects of hysiological concentrations of E 2 alone and the cellular and molecular mechanism(s) underlying estrogenic effects on mediator release from mast cells require further investigations.…”

Section: Introductionmentioning

confidence: 99%

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx

Zaitsu

Narita

Lambert

et al. 2007

Molecular Immunology

226

183

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Background-Allergic airway diseases are more common in females than in males during early adulthood. A relationship between female hormones and asthma prevalence and severity has been suggested, but the cellular and molecular mechanisms are not understood.Objective-To elucidate the mechanism(s) by which estrogens enhance the synthesis and release of mediators of acute hypersensitivity.Methods-Two mast cell/basophil cell lines (RBL-2H3 and HMC-1) and primary cultures of bone marrow derived mast cells, all of which naturally express estrogen receptor-α, were examined. Cells were incubated with physiological concentrations of 17-β-estradiol with and without IgE and allergens. Intracellular Ca 2+ concentrations and the release of β-hexosaminidase and leukotriene C 4 were quantified.Results-Estradiol alone induced partial release of the preformed, granular protein β-hexosaminidase from RBL-2H3, BMMC and HMC-1, but not from BMMC derived from estrogen receptor-α knock-out mice. The newly synthesized LTC 4 was also released from RBL-2H3. Estradiol also enhanced IgE-induced degranulation and potentiated LTC 4 production. Intracellular Ca 2+ concentration increased prior to and in parallel with mediator release. Estrogen receptor antagonists or Ca 2+ chelation inhibited these estrogenic effects.Conclusion-Binding of physiological concentrations of estradiol to a membrane estrogen receptor-α initiates a rapid onset and progressive influx of extracellular Ca 2+ , which supports the synthesis and release of allergic mediators. Estradiol also enhances IgE-dependent mast cell activation, resulting in a shift of the allergen dose response.

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“…Estrogen promotes MC degranulation and histamine release and enhances the IgE-dependent MC activation. Since it has been shown that MCs express estrogen receptors and E 2 enhances MC degranulation by genomic and non-genomic pathways (Cocchiara et al 1992, Zaitsu et al 2006), we could not discard the hypothesis that the MCs degranulation process and the consequent VEGF increase described here could be regulated by E 2 . Further investigations are necessary to elucidate this event.…”

Section: Discussionmentioning

confidence: 73%

Mast cell degranulation in rat uterine cervix during pregnancy correlates with expression of vascular endothelial growth factor mRNA and angiogenesis

Bosquiazzo¹,

Ramos²,

Varayoud³

et al. 2007

Reproduction

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Vascular growth of the uterine cervix during pregnancy is associated with mast cell (MC) degranulation. To better understand the mechanism underlying this process, uterine cervices of intact pregnant rats were dissected and endothelial cell proliferation was measured by a bromodeoxyuridine incorporation technique. Total vascular endothelial growth factor (VEGF) mRNA expression and the relative abundance of VEGF splice variants (120, 164, and 188) were determined by RT-PCR. VEGF protein expression was evaluated by immunohistochemistry. To investigate the role of MCs on cervical angiogenesis, a second set of pregnant animals were treated with an MC stabilizer (disodium cromoglycate) to inhibit MC degranulation. Furthermore, 17b-estradiol (E 2 ) serum levels were established by RIA. In intact pregnant rats, VEGF mRNA expression was positively correlated with endothelial cell proliferation and circulating E 2 levels. All selected splice variants of VEGF gene were detected and their relative abundance did not show any change throughout pregnancy. Animals treated with disodium cromoglycate showed a decrease in endothelial cell proliferation and in VEGF mRNA expression compared with controls. Relative abundance of VEGF mRNA splice variants and E 2 serum levels showed no differences between these experimental groups. These results show a time-dependent correlation between VEGF mRNA expression and E 2 serum levels in the uterine cervix of intact pregnant rats, while MC stabilizer-treated animals reduced the VEGF expression without modifying E 2 serum levels. We suggest that cervical angiogenesis during pregnancy could be regulated by a mechanism which involves endogenous E 2 and chemical mediators stored in MC granules via a VEGFdependent pathway.

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Oestradiol enhances in vitro the histamine release induced by embryonic histamine-releasing factor (EHRF) from uterine mast cells

Cited by 46 publications

References 2 publications

Relaxin, a Potent Microcirculatory Effector, Is Not Angiogenic

Relaxin, a Potent Microcirculatory Effector, Is Not Angiogenic

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx

Mast cell degranulation in rat uterine cervix during pregnancy correlates with expression of vascular endothelial growth factor mRNA and angiogenesis

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