Evidence That Formation of Vimentin·Mitogen-activated Protein Kinase (MAPK) Complex Mediates Mast Cell Activation following FcεRI/CC Chemokine Receptor 1 Cross-talk

Toda, Masako; Kuo, Chuan Hui; Borman, Satty; Richardson, Ricardo M.; Inoko, Akihito; Inagaki, Masaki; Collins, Andrea; Schneider, Klaus; Ono, Santa Jeremy

doi:10.1074/jbc.m111.319624

Cited by 26 publications

(26 citation statements)

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“…Activation of MAP kinases is known to be essential for IgEmediated expression of chemokines, cytokines, and eicosanoids in basophils and mast cells (Gibbs et al, 2002;Miura et al, 1999;Toda et al, 2012). Our results showed that IgE in the absence of allergens could induce phosphorylation of MAP kinases including JNK, p38 kinase, and ERK in RBL-2H3 cells.…”

Section: Discussionsupporting

confidence: 52%

IgE in the absence of allergen induces the expression of monocyte chemoattractant protein-1 in the rat basophilic cell-line RBL-2H3

Ahn

Jeon

Kang

et al. 2014

Molecular Immunology

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Section: Discussionsupporting

confidence: 52%

IgE in the absence of allergen induces the expression of monocyte chemoattractant protein-1 in the rat basophilic cell-line RBL-2H3

Ahn

Jeon

Kang

et al. 2014

Molecular Immunology

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“…Vimentin is involved in a variety of cellular processes, including vesicular membrane transport [6,7], signal transduction [8,9] and cell motility [10]. Similar to NPC1 cells, cells lacking vimentin are unable to transport LDL-derived cholesterol from their lysosomes to the endoplasmic reticulum for esterification [11].…”

Section: Introductionmentioning

confidence: 99%

PKC Activation in Niemann Pick C1 Cells Restores Subcellular Cholesterol Transport

Tamari

Chen

et al. 2013

PLoS ONE

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Activation of protein kinase C (PKC) has previously been shown to ameliorate the cholesterol transport defect in Niemann Pick Type C1 (NPC1) cells, presumably by increasing the soluble levels of one of its substrates, vimentin. This activity would then restore the vimentin cycle in these cells and allow vimentin-dependent retrograde transport to proceed. Here, we further investigate the effects of PKC activation in NPC1 cells by evaluating different isoforms for their ability to solubilize vimentin and correct the NPC1 cholesterol storage phenotype. We also examine the effects of PKC activators, including free fatty acids and the PKC-specific activator diazoxide, on the NPC1 disease phenotype. Our results indicate that PKC isoforms α, βII, and ε have the greatest effects on vimentin solubilization. Furthermore, expression or activation of PKCε in NPC1 cells dramatically reduces the amount of stored cholesterol and restores cholesterol transport out of endocytic vesicles. These results provide further support for the contribution of PKCs in NPC1 disease pathogenesis and suggest that PKCs may be targeted in future efforts to develop therapeutics for NPC1 disease.

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“…We demonstrated previously that immediate cellular responses to costimulation of CCR1 and FcεRI include phosphorylation of p38 MAPK and production of the intermediate filament vimentin (22). We are particularly interested in the chemokines and cytokines produced in response to mast cell activation and identified genes that are upregulated in response to costimulation of FcεRI and CCR1 on mast cells.…”

mentioning

confidence: 99%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 and CCR3; CCL7 is a ligand for these receptors. Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigated the requirement for CCL7 in a murine model of IgE-mediated allergic conjunctivitis. For mast cells treated with IgE and Ag, the presence of CCL7 synergistically enhanced degranulation and calcium influx. CCL7 also induced chemotaxis in mast cells. CCL7-deficient bone marrow–derived mast cells showed decreased degranulation following IgE and Ag treatment compared with wild-type bone marrow–derived mast cells, but there was no difference in degranulation when cells were activated via an IgE-independent pathway. In vivo, CCL7 was upregulated in conjunctival tissue during an OVA-induced allergic response. Notably, the early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized wild-type mice than in control challenged wild-type mice; the increase was suppressed in CCL7-deficient mice. In the OVA-induced allergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wild-type mice. Our results demonstrate that CCL7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcεRI-mediated mast cell activation in vitro. A better understanding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

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Evidence That Formation of Vimentin·Mitogen-activated Protein Kinase (MAPK) Complex Mediates Mast Cell Activation following FcεRI/CC Chemokine Receptor 1 Cross-talk

Cited by 26 publications

References 50 publications

IgE in the absence of allergen induces the expression of monocyte chemoattractant protein-1 in the rat basophilic cell-line RBL-2H3

IgE in the absence of allergen induces the expression of monocyte chemoattractant protein-1 in the rat basophilic cell-line RBL-2H3

PKC Activation in Niemann Pick C1 Cells Restores Subcellular Cholesterol Transport

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

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