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. 2014 Jan 17;443(3):980-6.
doi: 10.1016/j.bbrc.2013.12.078. Epub 2013 Dec 19.

miR-142-3p enhances FcεRI-mediated degranulation in mast cells

Yoji Yamada  1 , Kyoko Kosaka  1 , Tatsuya Miyazawa  1 , Kazumi Kurata-Miura  1 , Tetsuo Yoshida  2
Affiliations

miR-142-3p enhances FcεRI-mediated degranulation in mast cells

Yoji Yamada et al. Biochem Biophys Res Commun. .

Abstract

Mast cells are immune cells derived from hematopoietic progenitors. When they are activated by stimuli, they immediately release granule-associated mediators, leading to allergic inflammation. Several factors controlling mediator release have been identified; however, little is known whether microRNAs (miRNAs) are involved in this process. miRNAs are a small class of non-coding RNAs that negatively regulate gene expression. In this study, we investigated the relationship between miRNAs and degranulation in LAD2 cells, a human mast cell line. We demonstrated that silencing of Dicer, a key enzyme of miRNA biogenesis, attenuates degranulation, indicating that miRNAs are involved in mast cell degranulation. We furthermore discovered that the overexpression of miR-142-3p enhances FcεRI-mediated degranulation and that miR-142-3p rescues the reduction of degranulation by silencing Dicer. Similar effects were observed in bone marrow-derived mast cells obtained miR-142-3p-deficient mice. Our studies suggest that miR-142-3p is a potential therapeutic target in pathological conditions caused by mast cells, such as mastocytosis and allergies.

Keywords: Degranulation; Mast cell; miR-142-3p; microRNA.

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