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Micro RNA expression profiling of human blood monocyte subsets highlights functional differences
Author(s) -
Dang TruongMinh,
Wong WingCheong,
Ong SiewMin,
Li Peng,
Lum Josephine,
Chen Jinmiao,
Poidinger Michael,
Zolezzi Francesca,
Wong SiewCheng
Publication year - 2015
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12456
Subject(s) - microrna , biology , monocyte , cd16 , gene expression profiling , gene expression , microbiology and biotechnology , microarray analysis techniques , microarray , regulation of gene expression , gene , immunology , immune system , genetics , cd3 , cd8
Summary Within human blood there are two subsets of monocytes that can be identified by differential expression of CD 16. Although numerous phenotypic and functional differences between the subsets have been described, little is known of the mechanisms underlying the distinctive properties of the two subsets. Micro RNA s (mi RNA s) are small non‐coding RNA s that can regulate gene expression through promoting mRNA degradation or repressing translation, leading to alterations in cellular processes. Their potential influence on the functions of monocyte subsets has not been investigated. In this study, we employed microarray analysis to define the mi RNA expression profile of human monocyte subsets. We identified 66 mi RNA s that were differentially expressed ( DE ) between CD 16 + and CD 16 − monocytes. Gene ontology analysis revealed that the predicted targets of the DE mi RNA s were predominantly associated with cell death and cellular movement. We validated the functional impacts of selected DE mi RNA s in CD 16 − monocytes, over‐expression of miR‐432 significantly increases apoptosis, and inhibiting miR‐19a significantly reduces cell motility. Furthermore, we found that miR‐345, another DE mi RNA directly targets the transcription factor RelA in monocytes, which resulted in the differential expression of RelA in monocyte subsets. This implicates miR‐345 indirect regulation of many genes downstream of RelA, including important inflammatory mediators. Together, our data show that DE mi RNA s could contribute substantially to regulating the functions of human blood monocytes.