The role of histamine in platelet aggregation by physiological and immunological stimuli

Masini, Emanuela; Bello, M. G. Di; Raspanti, Silvia; Ndisang, J. Fomusi; Baronti, Roberto; Cappugi, Pietro; Mannaioni, P. F.

doi:10.1007/s000110050319

Cited by 44 publications

(40 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Histidine decarboxylase activity was assayed by measuring [ ) according to the method described previously (33). Determinations were done in quintuplicate.…”

Section: Methodsmentioning

confidence: 99%

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

Cianchi

Cortesini

Schiavone³

et al. 2005

Clinical Cancer Research

104

View full text Add to dashboard Cite

Purpose: Activity of histidine decarboxylase, the key enzyme in the synthesis of histamine, has been shown to be increased in several types of human tumors.We attempted to establish whether the possible involvement of histidine decarboxylase and histamine in colorectal carcinogenesis might be mediated by the activation of the cyclooxygenase-2 (COX-2) pathway. Experimental Design: Expression/activity of histidine decarboxylase, histamine content, and prostaglandin E 2 (PGE 2 ) production were analyzed in 33 colorectal cancer samples and in the HT29, Caco-2, and HCT116 colon cancer cell lines. The effects of histamine, celecoxib, and H 1 , H 2 , and H 4 receptor antagonists on COX-2 expression/activity, cell proliferation, and vascular endothelial growth factor (VEGF) production were assessed in the three colon cancer lines that showed different constitutive COX-2 expression. Results: We showed the up-regulation of histidine decarboxylase protein expression and activity in the tumor specimens when compared with normal colonic mucosa. Histidine decarboxylase activity and histamine content were also significantly higher in metastatic tumors than in nonmetastatic ones.These variables significantly correlated with tumor PGE 2 production.The administration of histamine increased COX-2 expression/activity, cell proliferation, and VEGF production in the COX-2-positive HT29 and Caco-2 cells. Treatment with either H 2 /H 4 receptor antagonists or celecoxib prevented these effects. Histamine had no effect on both the COX-2 pathway andVEGF production in the COX-2-negative HCT116 cells. Conclusions: Our data showed that histamine exerts both a proproliferative and a proangiogenic effect via H 2 /H 4 receptor activation. These effects are likely to be mediated by increasing COX-2-related PGE 2 production in COX-2-expressing colon cancer cells.

show abstract

“…Histidine decarboxylase activity was assayed by measuring [ ) according to the method described previously (33). Determinations were done in quintuplicate.…”

Section: Methodsmentioning

confidence: 99%

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

Cianchi

Cortesini

Schiavone³

et al. 2005

Clinical Cancer Research

104

View full text Add to dashboard Cite

show abstract

“…Histidine decarboxylase activity was assayed by measuring 14 CO 2 evolved from L-[carboxyl 14 C]-histidine (46 mCi/mmol, Amersham, England) using a previously reported method [4]. Histamine content was determined after a buthanol/heptane extraction from the tissue, using a fluorometric method as previously reported [5].…”

Section: Biochemical Determinations Immunostaining and Microvessel Cmentioning

confidence: 99%

“…These actions are mediated by the activation of specific histamine receptors, namely H 1 , H 2 , H 3 and H 4 . Histamine levels in cells and in tissues are regulated by the activity of histidine decarboxylase (HDC), that is the only enzyme responsible for the generation of histamine from L-histidine [1].…”

Section: Introductionmentioning

confidence: 99%

Histamine and histidine decarboxylase up-regulation in colorectal cancer: correlation with tumor stage

et al. 2005

Self Cite

View full text Add to dashboard Cite

“…6 Histamine also can activate platelets, and it potentiates the aggregatory response of other agonists including adrenaline, 5-hydroxytryptamine, and thrombin. [7][8][9] Moreover, histamine is able to modulate the activity of inflammatory cells such as neutrophils, 10 monocytes, 11 and eosinophils. 12 In urban environments, diesel exhaust particles (DEP) are one of the main contributors of atmospheric particulate matter of diameter Ͻ2.5 m (PM 2.5 ).…”

mentioning

confidence: 99%

Pharmacological Stabilization of Mast Cells Abrogates Late Thrombotic Events Induced by Diesel Exhaust Particles in Hamsters

et al. 2004

View full text Add to dashboard Cite

Background-Particulate air pollution is associated with cardiovascular diseases and myocardial infarction (MI). Methods and Results-We investigated the relationship between airway inflammation and thrombosis 24 hours after intratracheal (IT) instillation of diesel exhaust particles (DEP; 50 g/hamster). Mild thrombosis was induced in the femoral vein by endothelial injury, and the consequences of airway inflammation on thrombogenicity were studied via online video microscopy. Lung inflammation and histamine analysis in bronchoalveolar lavage (BAL) and plasma were performed after pretreatment with dexamethasone (DEX) or sodium cromoglycate (SC). DEP induced airway inflammation and histamine release in BAL and in plasma, and increased thrombosis, without elevating plasma von Willebrand factor (vWF) levels. The IT instillation of 400-nm positively charged polystyrene particles (500 g/hamster), serving as particles that do not penetrate into the circulation, equally produced airway inflammation, histamine release, and enhanced thrombosis. Histamine in plasma resulted from basophil activation. Intraperitoneal (IP) pretreatment with DEX (5 mg/kg) abolished the DEP-induced histamine increase in BAL and plasma and abrogated airway inflammation and thrombogenicity. The IT pretreatment with DEX (0.5 mg/kg) showed a partial but parallel inhibition of all of these parameters. Pretreatment with SC (40 mg/kg, IP) strongly inhibited airway inflammation, thrombogenicity, and histamine release. Conclusions-Our results are compatible with the triggering of mast cell degranulation and histamine release by DEP.Histamine plays an initial central role in airway inflammation, further release of histamine by circulating basophils, and peripheral thrombotic events. Antiinflammatory pretreatment can abrogate the peripheral thrombogenicity by preventing histamine release from mast cells.

show abstract

The role of histamine in platelet aggregation by physiological and immunological stimuli

Abstract: The synergistic effect between histamine and other monoamines on platelet aggregation may explain some aspects of allergic vasculitis in which platelet aggregation is present.

Cited by 44 publications

References 39 publications

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

Histamine and histidine decarboxylase up-regulation in colorectal cancer: correlation with tumor stage

Pharmacological Stabilization of Mast Cells Abrogates Late Thrombotic Events Induced by Diesel Exhaust Particles in Hamsters

Contact Info

Product

Resources

About