| First Author | Yamada Y | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 443 |
| Issue | 3 | Pages | 980-6 |
| PubMed ID | 24361879 | Mgi Jnum | J:211850 |
| Mgi Id | MGI:5576807 | Doi | 10.1016/j.bbrc.2013.12.078 |
| Citation | Yamada Y, et al. (2014) miR-142-3p enhances FcepsilonRI-mediated degranulation in mast cells. Biochem Biophys Res Commun 443(3):980-6 |
| abstractText | 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 FcepsilonRI-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. |
