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MiR-142-3p is a RANKL-dependent inducer of cell death in osteoclasts

MicroRNA are small, non-coding, single-stranded RNAs that are estimated to regulate ~60% of the human genome. MiRNA profiling of monocyte-to-osteoclast differentiation identified miR-142-3p as a miRNA that is significantly, differentially expressed throughout osteoclastogenesis. Enforced expression...

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Detalles Bibliográficos
Autores principales: Fordham, Jezrom B., Guilfoyle, Katherine, Naqvi, Afsar Raza, Nares, Salvador
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844978/
https://www.ncbi.nlm.nih.gov/pubmed/27113904
http://dx.doi.org/10.1038/srep24980
Descripción
Sumario:MicroRNA are small, non-coding, single-stranded RNAs that are estimated to regulate ~60% of the human genome. MiRNA profiling of monocyte-to-osteoclast differentiation identified miR-142-3p as a miRNA that is significantly, differentially expressed throughout osteoclastogenesis. Enforced expression of miR-142-3p via transient transfection with miR-142-3p mimic inhibited cell-to-cell contact and fusion, decreased protein kinase C alpha expression, and ultimately reduced cell viability. miR-142-3p was also identified as significantly differentially expressed during monocyte-to-macrophage differentiation and overexpression of miR-142-3p prevented their conversion to osteoclasts. Furthermore, the inhibitory effect of miR-142-3p on osteoclastogenesis extended to the conversion of a third osteoclast precursor cell type- dendritic cells. These results demonstrate miR-142-3p to be a negative regulator of osteoclastogenesis from the 3 main precursor cell types: monocytes, macrophages and dendritic cells. Importantly, decreased survival was dependent upon both miR-142-3p expression and RANK-signaling, with no harmful effects detected in the absence of this combination. As such, miR-142-3p represents a novel target for the selective removal of osteoclasts by targeting of osteoclastogenic pathways.