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Mast cell function is not altered by Coronin-1A deficiency.

ABSTRACT: Coronin-1A is a WD repeat protein family member, highly expressed in all hematopoietic lineages, and acts as a regulator of F-actin dynamics and Ca2+ signaling. In Coro1a(Lmb3) mice results in inactivation of the protein and leads to disease resistance in a model of lupus erythematosus. In Coro1a(-/-) and Coro1a(Lmb3) mice, peripheral T cells exhibit impairments in survival, migration, activation, and Ca2+ flux. In this study, we show that in vitro-differentiated mast cells from Coro1a(Lmb3) mice are viable, developed normally, and are fully functional in assays of degranulation, cytokine secretion, and chemotactic migration, despite increased F-actin levels. In Coro1a(Lmb3) mast cells, Ca2+ flux in response to physiological Fc?RI stimulation is unaffected. Finally, Coro1a(Lmb3) mice showed similar in vivo mast cell responses as the WT mice. Coronin-1B and Coronin-1C expression levels were not increased in Coro1a(Lmb3) mast cells but were higher in mast cells than in CD4 T cells or B cells in WT mice. We conclude that Coronin-1A activity is not required for mast cell function.

SUBMITTER: Arandjelovic S

PROVIDER: S-EPMC2974433 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature

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Mast cell function is not altered by Coronin-1A deficiency.

Arandjelovic Sanja S Wickramarachchi Dilki D Hemmers Saskia S Leming Sunamita S SS Kono Dwight H DH Mowen Kerri A KA

Journal of leukocyte biology 20100719 4

Coronin-1A is a WD repeat protein family member, highly expressed in all hematopoietic lineages, and acts as a regulator of F-actin dynamics and Ca2+ signaling. In Coro1a(Lmb3) mice results in inactivation of the protein and leads to disease resistance in a model of lupus erythematosus. In Coro1a(-/-) and Coro1a(Lmb3) mice, peripheral T cells exhibit impairments in survival, migration, activation, and Ca2+ flux. In this study, we show that in vitro-differentiated mast cells from Coro1a(Lmb3) mic ...[more]

PMID: 20643816

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Project description:Mast cells are highly versatile cells that perform a variety of functions depending on the immune trigger, context of activation, and cytokine stimulus. Antigen-mediated mast cell responses are regulated by transcriptional processes that result in the induction of numerous genes contributing to mast cell function. Recently, we also showed that exposure to dietary agents with known epigenetic actions such as curcumin can suppress mast cell-mediated food allergy, suggesting that mast cell responses in vivo may be epigenetically regulated. To further assess the effects of epigenetic modifications on mast cell function, we examined the behavior of bone marrow-derived mast cells (BMMCs) in response to trichostatin A (TSA) treatment, a well-studied histone deacetylase inhibitor. IgE-mediated BMMC activation resulted in enhanced expression and secretion of IL-4, IL-6, TNF-?, and IL-13. In contrast, pretreatment with TSA resulted in altered cytokine secretion. This was accompanied by decreased expression of Fc?RI and mast cell degranulation. Interestingly, exposure to non-IgE stimuli such as IL-33, was also affected by TSA treatment. Furthermore, continuous TSA exposure contributed to mast cell apoptosis and a decrease in survival. Further examination revealed an increase in I-?B? and a decrease in phospho-relA levels in TSA-treated BMMCs, suggesting that TSA alters transcriptional processes, resulting in enhancement of I-?B? transcription and decreased NF-?B activation. Lastly, treatment of wild-type mice with TSA in a model of ovalbumin-induced food allergy resulted in a significant attenuation in the development of food allergy symptoms including decreases in allergic diarrhea and mast cell activation. These data therefore suggest that the epigenetic regulation of mast cell activation during immune responses may occur via altered histone acetylation, and that exposure to dietary substances may induce epigenetic modifications that modulate mast cell function.

Dataset Information

Mast cell function is not altered by Coronin-1A deficiency.

Publications

Mast cell function is not altered by Coronin-1A deficiency.

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