Histamine formed in stimulated human platelets is cytoplasmic

Saxena, Satya; McNicol, Archibald; Brandes, Lorne J.; Becker, Allan B.; Gerrard, Jon M.

doi:10.1016/0006-291x(89)91697-5

Cited by 21 publications

(10 citation statements)

References 9 publications

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“…However, using 5-HT as example, a spectrum of phenomena cannot be explained by GPCR signaling, particularly the above-mentioned pulmonary artery smooth muscle cell hyperplasia, which can be abolished by SERT blockade with 5-HT-specific re-uptake inhibitors, such as fluoxetine, but not with 5-HT receptor antagonists, suggesting an intracellular role for 5-HT [47,48]. Such phenomena are known for all PBMAs [49][50][51][52][53][54][55][56][57] but in most cases the underlying mechanisms remain unknown.…”

Section: The Duality Of the Serotonergic Systemmentioning

confidence: 99%

Novel roles for biogenic monoamines: from monoamines in transglutaminase‐mediated post‐translational protein modification to monoaminylation deregulation diseases

2011

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Functional protein serotonylation is a newly recognized post-translational modification with the primary biogenic monoamine (PBMA) serotonin (5-HT). This covalent protein modification is catalyzed by transglutaminases (TGs) and, for example, acts in the constitutive activation of small GTPases. Multiple physiological roles have been identified since its description in 2003 and, importantly, deregulated serotonylation was shown in the etiology of bleeding disorders, primary pulmonary hypertension and diabetes. The PBMAs 5-HT, histamine, dopamine, and norepinephrine all act as neurotransmitters in the nervous system and as hormones in non-neuronal tissues, which points out their physiological importance. In analogy to serotonylation we have found that also the other PBMAs act through the TG-catalyzed mechanisms of 'histaminylation', 'dopaminylation' and 'norepinephrinylation'. Therefore, PBMAs deploy a considerable portion of their effects via protein monoaminylation in addition to their canonical receptor-mediated signaling. Here, the implications of these newly identified post-translational modifications are presented and discussed. Furthermore, the potential regulatory roles of protein monoaminylation in small GTPase, heterotrimeric G-protein and lipid signaling, as well as in modulating metabolic enzymes and nuclear processes, are critically assessed.

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Section: The Duality Of the Serotonergic Systemmentioning

confidence: 99%

Novel roles for biogenic monoamines: from monoamines in transglutaminase‐mediated post‐translational protein modification to monoaminylation deregulation diseases

2011

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“…Human platelets are capable of synthesizing and releasing histamine [38], and platelets may also induce the release of histamine from mast cells and basophils through IgEdependent mechanisms, resulting in bronchoconstriction [39]. Other pleiotropic inflammatory mediators released by activated platelets, e.g.…”

Section: Direct Pathological Effects Of Platelets On Inflamed Tissuementioning

confidence: 99%

Defining a role for platelets in allergic inflammation

Pitchford

2007

Biochemical Society Transactions

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There is now considerable evidence suggesting a role for platelets as inflammatory cells. These actions are distinct from their classically known actions performed during thrombosis and haemostasis, and include the expression of adhesion molecules and contact-dependent activation of leucocytes, the release of a plethora of inflammatory mediators, activation in cells of the adaptive immune response and the ability to migrate and undergo chemotaxis. Chronic asthma is a disease characterized by a mixed inflammatory cell pulmonary infiltrate, AHR (airways hyper-responsiveness) and tissue remodelling. Clinical data from patients suffering from asthma, allergic rhinitis and allergic dermatitis reveal changes in platelet behaviour and function during or after allergen exposure. Furthermore, mouse models of allergic inflammation demonstrate a role for intact platelets in eosinophil and lymphocyte recruitment to the lungs, a mechanism that is P-selectin (platelet selectin)-dependent. Models of chronic inflammation also reveal the participation of platelets in tissue remodelling events whereby platelet depletion was found to be more effective in suppressing airway remodelling processes than the administration of a glucocorticosteroid. This process of destruction and repair to the architecture of airway tissue is therefore perhaps enhanced by platelet activation. Recent evidence demonstrates that platelets can undergo chemotaxis and indicates an ability to migrate through inflamed tissue, where they localize to specific tissue sites. Indeed, platelets have been shown to become activated and recruited to various body compartments in direct response to allergen via IgE and this is suggestive of a link between the innate and adaptive immune responses. Thus these actions may lead to pathophysiological events that alter disease progression, since platelet depletion suppresses AHR in allergic rabbits. Further investigations into the role of platelets in inflammation may be beneficial in the search for future therapeutic targets in the treatment of asthma and allergy.

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“…However, other cell types, such as DCs and lymphocytes, do not store histamine intracellularly but secrete it after synthesis. [11][12][13] Although histamine is well recognized for its effects in the immediate-type hypersensitivity response (ie, increased vascular permeability, smooth muscle contraction, activation of nociceptive nerves, wheal-and-flare reaction, and itch response), the pathological relevance of increased histamine levels at diseased sites is less well understood in other disorders, such as inflammatory bowel disease and irritable bowel syndrome. 14,15 Indeed, histamine might negatively or positively influence parasitic or bacterial infections.…”

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confidence: 99%