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- Title
MicroRNA-101a regulates microglial morphology and inflammation.
- Authors
Reiko Saika; Hiroshi Sakuma; Daisuke Noto; Shuhei Yamaguchi; Takashi Yamamura; Sachiko Miyake; Saika, Reiko; Sakuma, Hiroshi; Noto, Daisuke; Yamaguchi, Shuhei; Yamamura, Takashi; Miyake, Sachiko
- Abstract
<bold>Background: </bold>Microglia, as well as other tissue-resident macrophages, arise from yolk sac progenitors. Thus, it is likely that the central nervous system environment is critical for the acquisition of a distinct microglial phenotype. Several microRNAs that are enriched in the brain play crucial roles in brain development and may also play a role in the differentiation of microglia.<bold>Methods: </bold>To track the differentiation of hematopoietic cells into microglia, lineage-negative bone marrow cells were co-cultured with astrocytes in the absence or presence of microRNAs or their inhibitors. Microglia-like cells were identified as small, round cells that were immunopositive for CD11b, Iba1, CX3CR1, and triggering receptor expressed on myeloid cells (TREM)-2.<bold>Results: </bold>Five microRNAs (miR-101a, miR-139-3p, miR-214*, miR-218, and miR-1186) were identified as modifiers of the differentiation of bone marrow-derived microglia-like cells. Among them, miR-101a facilitated the differentiation of bone marrow cells into microglia-like cells most potently. Small, round cells expressing CD11b, Iba1, CX3CR1, and TREM-2 were predominant in cells treated by miR-101a. miR-101a was abundantly expressed in non-microglial brain cells. Transfection of miR-101a into microglia significantly increased the production of IL-6 in response to LPS. Finally, miR-101a downregulated the expression of MAPK phosphatase-1.<bold>Conclusions: </bold>miR-101a, which is enriched in the brain, promotes the differentiation of bone marrow cells into microglia-like cells.
- Subjects
MICROGLIA; MICRORNA; INFLAMMATION; BONE marrow cells; MITOGEN-activated protein kinase phosphatases; CELL metabolism; PROTEIN metabolism; RNA metabolism; ANALYSIS of variance; ANIMAL experimentation; ANIMAL populations; BIOLOGICAL models; CALCIUM-binding proteins; CELL culture; CELL differentiation; CELL physiology; CELL receptors; CELLS; CELLULAR signal transduction; GENETIC techniques; MACROPHAGES; RESEARCH methodology; MICE; MICROFILAMENT proteins; NUCLEOTIDES; PROTEINS; RNA; TISSUE culture
- Publication
Journal of Neuroinflammation, 2017, Vol 14, p1
- ISSN
1742-2094
- Publication type
journal article
- DOI
10.1186/s12974-017-0884-8