Mediator release from mast cells by nerve growth factor. Neurotrophin specificity and receptor mediation

Horigome, Kazuhiko; Pryor, John C.; Bullock, E D; Johnson, Eugene M.

doi:10.1016/s0021-9258(18)82415-2

Cited by 217 publications

(12 citation statements)

References 51 publications

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“…NGF can also exert effects via indirect interactions with a number of different cell types in peripheral tissues, including mast cells, leukocytes and sympathetic neurons. 72–77 In response to NGF, these can release a variety of substances, including inflammatory mediators that directly affect ion channels and receptors on peripheral nerve endings. Importantly, most of these cell types are resident in bone marrow, or can be recruited to bone marrow under pathological conditions such as inflammation.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain

et al. 2017

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Sequestration of nerve growth factor has been used successfully in the management of pain in animal models of bone disease and in human osteoarthritis. However, the mechanisms of nerve growth factor-induced bone pain and its role in modulating inflammatory bone pain remain to be determined. In this study, we show that nerve growth factor receptors (TrkA and p75) and some other nerve growth factor-signaling molecules (TRPV1 and Nav1.8, but not Nav1.9) are expressed in substantial proportions of rat bone nociceptors. We demonstrate that nerve growth factor injected directly into rat tibia rapidly activates and sensitizes bone nociceptors and produces acute behavioral responses with a similar time course. The nerve growth factor-induced changes in the activity and sensitivity of bone nociceptors we report are dependent on signaling through the TrkA receptor, but are not affected by mast cell stabilization. We failed to show evidence for longer term changes in expression of TrkA, TRPV1, Nav1.8 or Nav1.9 in the soma of bone nociceptors in a rat model of inflammatory bone pain. Thus, retrograde transport of NGF/TrkA and increased expression of some of the common nerve growth factor signaling molecules do not appear to be important for the maintenance of inflammatory bone pain. The findings are relevant to understand the basis of nerve growth factor sequestration and other therapies directed at nerve growth factor signaling, in managing pain in bone disease.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain

et al. 2017

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“…[135][136][137] Nerve growth factor may directly or indirectly affect tissue immune reactivity. Indirect effects of NGF may result from its cytokinelike actions, including stimulation of the release of inflammatory mediators from lymphocytes 138,139 and degranulation of mast cells. 140 Furthermore, NGF is capable of directly modulating neuropeptide expression in tyrosine kinase-expressing neurons.…”

Section: Nerve Growth Factormentioning

confidence: 99%

Neuropeptides

Schäffer¹,

Beiter²,

Becker³

et al. 1998

Arch Surg

161

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uccessful repair of injured tissues requires diverse interactions between cells, biochemical mediators, and the cellular microenvironment. [1][2][3] Much has been learned about the individual events that are involved in this process, but their integration is clearly far more complex than has been imagined, and the important role of neurogenic stimuli is only recently being recognized.Neurogenic stimuli profoundly affect cellular events that are involved in inflammation, proliferation, and matrix, as well as cytokine and growth factor synthesis. Immune cells regulated by neuropeptides include lymphocyte subsets, macrophages, and mast cells. In addition, neuropeptides may affect the proliferative and synthetic activity of epithelial, vascular, and connective tissue cells. Furthermore, a close interaction between the nervous and the immune systems has become obvious. 4 The peripheral nervous system (PNS), acting through neuropeptides, not only relays sensory information to the central nervous system (CNS) but also plays an effector role in the inflammatory, proliferative, and reparative processes after injury. These effects range from growth factor and cytokine responses to control of local blood flow. Neuropeptides mediate many of the actions important in tissue-nervous system communication.We review the accumulated knowledge about the role of neuropeptides in inflammation as it pertains to tissue repair. NEUROPEPTIDES OF THE PNSNeuropeptides constitute one of the largest families of extracellular messengers, having a long phylogenetic history. They can act as neurotransmitters, hormones, and paracrine factors.

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“…However, there are other cellular elements in peripheral tissues which express the trkA receptor and it is therefore possible that sensitization of nociceptors arises indirectly. TrkA receptors are known to be expressed by both sympathetic postganglionic neurons and by some mast cells (Horigome et al 1993;Thoenen 1991), and indeed NGF is known to be a potent degranulator of mast cells (Horigome 1993). There is good evidence that mast cell products (such as histamine and serotonin) are capable of sensitizing nociceptors (see Reeh & Kress 1995).…”

Section: (*) the P Erip H Era L Sen Sitization O F N Ociceptorsmentioning

confidence: 99%

NGF as a mediator of inflammatory pain

1996

Phil. Trans. R. Soc. Lond. B

291

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The chapter reviews some of recent evidence which suggests that one neurotrophin, nerve growth factor (NGF), is a peripherally produced mediator of some persistent pain states, notably those associated with inflammation. The evidence for this proposal is as follows. 1. The endogenous production of NGF regulates the sensitivity of nociceptive systems. Behavioural and electrophysiological studies have shown that sequestration of constitutively produced NGF leads to decrease nociceptor sensitivity. 2. In a wide variety of experimental inflammatory conditions NGF levels are rapidly increased in the inflamed tissue. 3. The high-affinity NGF receptor, trkA, is selectively expressed by nociceptive sensory neurons particularly those containing sensory neuropeptides such as substance P and CGRP. 4. The systematic or local application of exogenous NGF produces a rapid and prolonged behavioural hyperalgesia in both animals and humans. Exogenous NGF has also been found to activate and sensitize fine calibre sensory neurons. 5. In a number of animal models, much of the hyperalgesia associated with experimental inflammation is blocked by pharmacological "antagonism' of NGF. The mechanisms by which NGF up-regulation in inflamed tissues might lead to sensory abnormalities is also discussed. In particular, evidence is reviewed which suggests that increased NGF levels leads to both peripheral sensitization of nociceptors and central sensitization of dorsal horn neurons responding to noxious stimuli.

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Mediator release from mast cells by nerve growth factor. Neurotrophin specificity and receptor mediation

Cited by 217 publications

References 51 publications

Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain

Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain

Neuropeptides

NGF as a mediator of inflammatory pain

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