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Updated: May 4, 2026
Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays
Published on: July 4, 2018
miR-142-3p enhances FcεRI-mediated degranulation in mast cells
Yoji Yamada1, Kyoko Kosaka1, Tatsuya Miyazawa1
1Biologics Research Laboratories, Kyowa Hakko Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo 194-8533, Japan.
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.
Insights
MicroRNAs regulate mast cell degranulation, a key process in allergic inflammation. Specifically, miR-142-3p enhances this process, offering a potential therapeutic target for mast cell-related disorders.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Mast cells are crucial immune cells involved in allergic inflammation through mediator release.
- MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression, but their role in mast cell degranulation is largely unknown.
Purpose of the Study:
- To investigate the role of miRNAs in mast cell degranulation.
- To identify specific miRNAs involved in the regulation of mast cell mediator release.
Main Methods:
- Utilized LAD2 cells (a human mast cell line) and bone marrow-derived mast cells from miR-142-3p-deficient mice.
- Manipulated Dicer expression to assess miRNA biogenesis impact on degranulation.
- Overexpressed miR-142-3p to evaluate its effect on FcεRI-mediated degranulation.
Main Results:
- Silencing Dicer, a key enzyme in miRNA synthesis, reduced mast cell degranulation.
- Overexpression of miR-142-3p enhanced FcεRI-mediated degranulation in mast cells.
- miR-142-3p expression rescued the degranulation defect caused by Dicer silencing.
- Similar effects were observed in miR-142-3p-deficient mouse mast cells.
Conclusions:
- MicroRNAs, particularly miR-142-3p, play a significant role in regulating mast cell degranulation.
- miR-142-3p enhances FcεRI-mediated degranulation, suggesting its involvement in allergic responses.
- miR-142-3p represents a potential therapeutic target for mast cell-mediated diseases like allergies and mastocytosis.
