miR-142-3p acts as an essential modulator of neutrophil development in zebrafish

Abstract

Key Points The miR-142-3p double mutant zebrafish displayed aberrant neutrophil hypermaturation and homeostasis in myelopoiesis. Abnormal activation of IFN-γ signaling mediated the impaired neutrophil development in miR-142-3p–deficient zebrafish.

Altered lymphopoiesis and immunodeficiency in miR-142 null mice

“…Our conclusion is in agreement with observations by others that miR-142-3p and not miR-142-5p is responsible for the regulation of immune cell function in mice 12,13,35 and zebrafish. [9][10][11] Growing evidence suggests that miRNAs tightly control cellular responses and organismal homeostasis by targeting signaling nodes in a variety of physiological networks. In agreement with this notion, our study shows that miR-142-3p targets several signaling pathways that play well-established roles in B-cell differentiation and function, including the VDJ recombination complex, actin cytoskeleton rearrangement networks, and BAFF-R signaling cascade.…”

“…Knockdown of miR-142-3p expression in zebrafish revealed a critical role for this miRNA in hematopoiesis during embryonic development, hematopoietic stem cell homeostasis, neutrophil differentiation, and heart development. [9][10][11] In mice, miR-142 is essential for normal development and function of megakaryocytes, dendritic, and mast cells.…”

MiR-142 Is Required for Staphylococcus aureus Clearance at Skin Wound Sites via Small GTPase-Mediated Regulation of the Neutrophil Actin Cytoskeleton

“…The morphology of miR-142 −/− neutrophils appeared similar to that of neutrophils in zebrafish deficient in miR-142ab, in which these cells fail to developmentally disperse, suggesting that the migratory capacity of miR-142 in mammalian neutrophils might also be altered (Fan et al, 2014). To investigate the mechanisms of neutrophil chemotaxis, we incubated bone …”

RNA regulators of host immunity and pathogen adaptive responses in the oral cavity

“…Mir-142-3p was one of the few miRNAs found to be differentially regulated in three separate periodontitis studies. Its expression was previously demonstrated to be specific to cells of the hematopoietic lineage [53] and it functions in the differentiation and proliferation of immune cells as well the production of cytokines [28, 51, 102, 112, 125]. Since a similar increase in mir-142-3p expression was not observed in pulpitis and periapical disease, the higher mir-142-3p expression in gingival samples is likely as a result of a genuine differential regulation in periodontitis, rather than just an increased number of immune cells within the samples.…”