ADAM10 is required for SCF-induced mast cell migration

Faber, Travis; Pullen, Nick; Fernando, Josephine; Kolawole, Elizabeth Motunrayo; McLeod, Jamie Josephine Avila; Taruselli, Marcela T.; Williams, Kathryn L.; Rivera, Kevin O.; Barnstein, Brian; Conrad, Daniel H.; Ryan, John

doi:10.1016/j.cellimm.2014.05.005

Cited by 15 publications

(8 citation statements)

References 65 publications

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“…). ADAM 10 is pertinent to the development of allergy through multiple mechanisms . Our previous work with Der p 1 suggested that ADAM 10 activation lies downstream from ATP release and amplifies the conversion of prothrombin to thrombin .…”

Section: Discussionmentioning

confidence: 99%

Pathways of airway oxidant formation by house dust mite allergens and viral RNA converge through myosin motors, pannexons and Toll‐like receptor 4

Zhang

Chen

Mangat

et al. 2018

Immunity Inflam & Disease

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IntroductionIntracellular reactive oxidant species (ROS) are generated in human airway epithelial cells by the prothrombinase action of Group 1 house dust mite (HDM) allergens and by ligation of viral RNA sensor Toll‐like receptors (TLRs). We explored signaling convergence between HDM allergens and TLRs in ROS generation because epithelial cells form the primary barrier against inhaled substances and dictate host responses to allergens and viruses.MethodsROS formation by Calu‐3 human airway cells was studied by measuring dihydrorhodamine 123 oxidation after activation by polyinosinic:polycytidylic acid (to activate TLR3), CL097 (to activate TLR7), a natural mixture of HDM allergens, or BzATP.ResultsTLR4 activation was identified as an indispensable response element for all stimuli, operating downstream from myosin motor activation, pannexon gating for ATP release and the endogenous activation of prothrombin. Exogenous prothrombin activation by HDM allergens was prevented by SGUL 1733, a novel inhibitor of the proteolytic activity of Group 1 HDM allergens, which thus prevented TLR4 from being activated at source.ConclusionsOur data identify for the first time that endogenously‐generated prothrombin and TLR4 form a shared effector mechanism essential to intracellular ROS generation activated by a group 1 HDM allergen (itself a prothrombinase) or by ligation of viral RNA‐sensing TLRs. These stimuli operate a confluent signaling pathway in which myosin motors, gating of pannexons, and ADAM 10 lead to prothrombin‐dependent activation of TLR4 with a recycling activation of pannexons.

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Section: Discussionmentioning

confidence: 99%

Pathways of airway oxidant formation by house dust mite allergens and viral RNA converge through myosin motors, pannexons and Toll‐like receptor 4

Zhang

Chen

Mangat

et al. 2018

Immunity Inflam & Disease

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“…reported that ADAM10 was important for the progression of IgE‐dependent lung inflammation, suggesting that decreasing ADAM10 activity could be beneficial in controlling asthma and possibly other IgE‐dependent diseases. Furthermore, Faber et al . recently demonstrated a critical role for ADAM10 in the proliferation, differentiation, and migration of mast cells that was somewhat independent of IgE and ADAM17.…”

Section: Discussionmentioning

confidence: 99%

Expression profile of ADAM10 and ADAM17 in allergic rhinitis

Chueh

Park

Hur

et al. 2015

Int Forum Allergy Rhinol

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“…Common immunohistochemical (IHC) techniques for MCs identify granule-associated contents, ignoring populations of MCs that are not granulated, either due to immaturity or recent granule release. Additionally, MC degranulation releases SCF, a potent growth and chemotactic factor for MCs (13, 76), resulting in local proliferation (77) and recruitment (78). Therefore, increases in MC density may be due to activation of MCs from degranulation and not tissue damage.…”

Section: Mast Cells As Enhancers In Cardiac Fibrosismentioning

confidence: 99%

Mast Cells in Cardiac Fibrosis: New Insights Suggest Opportunities for Intervention

et al. 2019

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Mast cells (MC) are innate immune cells present in virtually all body tissues with key roles in allergic disease and host defense. MCs recognize damage-associated molecular patterns (DAMPs) through expression of multiple receptors including Toll-like receptors and the IL-33 receptor ST2. MCs can be activated to degranulate and release pre-formed mediators, to synthesize and secrete cytokines and chemokines without degranulation, and/or to produce lipid mediators. MC numbers are generally increased at sites of fibrosis. They are potent, resident, effector cells producing mediators that regulate the fibrotic process. The nature of the secretory products produced by MCs depend on micro-environmental signals and can be both pro- and anti-fibrotic. MCs have been repeatedly implicated in the pathogenesis of cardiac fibrosis and in angiogenic responses in hypoxic tissues, but these findings are controversial. Several rodent studies have indicated a protective role for MCs. MC-deficient mice have been reported to have poorer outcomes after coronary artery ligation and increased cardiac function upon MC reconstitution. In contrast, MCs have also been implicated as key drivers of fibrosis. MC stabilization during a hypertensive rat model and an atrial fibrillation mouse model rescued associated fibrosis. Discrepancies in the literature could be related to problems with mouse models of MC deficiency. To further complicate the issue, mice generally have a much lower density of MCs in their cardiac tissue than humans, and as such comparing MC deficient and MC containing mouse models is not necessarily reflective of the role of MCs in human disease. In this review, we will evaluate the literature regarding the role of MCs in cardiac fibrosis with an emphasis on what is known about MC biology, in this context. MCs have been well-studied in allergic disease and multiple pharmacological tools are available to regulate their function. We will identify potential opportunities to manipulate human MC function and the impact of their mediators with a view to preventing or reducing harmful fibrosis. Important therapeutic opportunities could arise from increased understanding of the impact of such potent, resident immune cells, with the ability to profoundly alter long term fibrotic processes.

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ADAM10 is required for SCF-induced mast cell migration

Cited by 15 publications

References 65 publications

Pathways of airway oxidant formation by house dust mite allergens and viral RNA converge through myosin motors, pannexons and Toll‐like receptor 4

Pathways of airway oxidant formation by house dust mite allergens and viral RNA converge through myosin motors, pannexons and Toll‐like receptor 4

Expression profile of ADAM10 and ADAM17 in allergic rhinitis

Mast Cells in Cardiac Fibrosis: New Insights Suggest Opportunities for Intervention

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