Mast cell regranulation requires a metabolic switch involving mTORC1 and a glucose-6-phosphate transporter

Iskarpatyoti, Jason A.; Shi, Jianling; Abraham, Mathew; Rathore, Abhay P. S.; Miao, Yanying; Abraham, Soman N.

doi:10.1016/j.celrep.2022.111346

Cited by 8 publications

(3 citation statements)

References 56 publications

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“…1 ), and additionally by the possibility of MCs taking up substances from their immediate environment and then re-releasing them. In this context, it has to be noted that MCs are able to survive even complete degranulation followed by regranulation (Iskarpatyoti et al 2022 ). Interestingly, MCs have altered granule contents and structure after regranulation, likely depending on the trigger that had induced the degranulation (Friend et al 1996 ; Iskarpatyoti et al 2022 , further references therein).…”

Section: Discussionmentioning

confidence: 99%

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

Molderings

Afrin

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Mast cells (MCs) occupy a central role in immunological as well as non-immunological processes as reflected in the variety of the mediators by which MCs influence other cells. Published lists of MC mediators have all shown only subsets—usually quite small—of the full repertoire. The full repertoire of MC mediators released by exocytosis is comprehensively compiled here for the first time. The compilation of the data is essentially based on the largely cytokine-focused database COPE®, supplemented with data on the expression of substances in human MCs published in several articles, plus extensive research in the PubMed database. Three hundred and ninety substances could be identified as mediators of human MCs which can be secreted into the extracellular space by activation of the MC. This number might still be an underestimate of the actual number of MC mediators since, in principle, all substances produced by MCs can become mediators because of the possibility of their release by diffusion into the extracellular space, mast cell extracellular traps, and intercellular exchange via nanotubules. When human MCs release mediators in inappropriate manners, this may lead to symptoms in any or all organs/tissues. Thus, such MC activation disorders may clinically present with a myriad of potential combinations of symptoms ranging from trivial to disabling or even life-threatening. The present compilation can be consulted by physicians when trying to gain clarity about MC mediators which may be involved in patients with MC disease symptoms refractory to most therapies.

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Section: Discussionmentioning

confidence: 99%

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

Molderings

Afrin

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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“…It is interesting to note that there is evidence for the participation of the mTORC1mediated signaling pathway in the process of MC granule biogenesis after degranulation [42]. Presumably, this effect is mediated by mTORC1-dependent activation of the transcription factor EB (TFEB), which regulates autophagy and lysosome biogenesis.…”

Section: Inhibition Of Autophagy Promotes MC Activationmentioning

confidence: 99%

The Role Played by Autophagy in FcεRI-Dependent Activation of Mast Cells

Pavlyuchenkova,

Smirnov,

Chernyak

et al. 2024

Cells

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The significant role of mast cells in the development of allergic and inflammatory diseases is well-established. Among the various mechanisms of mast cell activation, the interaction of antigens/allergens with IgE and the subsequent binding of this complex to the high-affinity IgE receptor FcεRI stand out as the most studied and fundamental pathways. This activation process leads to the rapid exocytosis of granules containing preformed mediators, followed by the production of newly synthesized mediators, including a diverse array of cytokines, chemokines, arachidonic acid metabolites, and more. While conventional approaches to allergy control primarily focus on allergen avoidance and the use of antihistamines (despite their associated side effects), there is increasing interest in exploring novel methods to modulate mast cell activity in modern medicine. Recent evidence suggests a role for autophagy in mast cell activation, offering potential avenues for utilizing low-molecular-weight autophagy regulators in the treatment of allergic diseases. More specifically, mitochondria, which play an important role in the regulation of autophagy as well as mast cell activation, emerge as promising targets for drug development. This review examines the existing literature regarding the involvement of the molecular machinery associated with autophagy in FcεRI-dependent mast cell activation.

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“…After the MCs have been activated, they degranulate and release the inflammatory mediators stored in their granules in seconds (rapid release) (27). However, most of the production of the potent inflammatory cytokine tumor necrosis factor (TNF) results from the induction of the corresponding mRNA upon MC activation (late secretion) (28).…”

Section: Introductionmentioning

confidence: 99%

Activation of Mast Cells by Neuropeptides: The Role of Pro-inflammatory and Anti-Inflammatory Cytokines

Lauritano¹,

Mastrangelo²,

D’Ovidio³

et al. 2023

Preprint

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Mass cells (MCs) are tissue cells that are derived from bone marrow stem cells that contribute to allergic reactions, inflammatory diseases, innate and adaptive immunity, autoimmunity, and mental disorders. MCs located near the meninges communicate with microglia through the production of mediators such as histamine and tryptase, but also through the secretion of IL-1, IL-6 and TNF, which can create pathological effects in the brain. Preformed chemical mediators of inflammation and tumor necrosis factor (TNF) are rapidly released from the granules of MCs, the only immune cells capable of storing the cytokine TNF, although it can also be produced later through mRNA. The role of MCs in nervous system diseases has been extensively studied and reported in scientific literature and is of great clinical interest. However, many of the published articles concern studies on animals (mainly rats or mice) and not on humans. MCs are known to interact with neuropeptides that mediate endothelial cell activation, resulting in central nervous system (CNS) inflammatory disorders. In the brain, MCs interact with neurons causing neuronal excitation with the production of neuropeptides and the release of inflammatory mediators such as cytokines and chemokines. This article explores the current understanding of MC activation by neuropeptides and the role of pro-inflammatory cytokines, suggesting a therapeutic effect of the anti-inflammatory cytokines IL-37 and IL-38.

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Mast cell regranulation requires a metabolic switch involving mTORC1 and a glucose-6-phosphate transporter

Cited by 8 publications

References 56 publications

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

The Role Played by Autophagy in FcεRI-Dependent Activation of Mast Cells

Activation of Mast Cells by Neuropeptides: The Role of Pro-inflammatory and Anti-Inflammatory Cytokines

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