Title

MicroRNA control of bone formation and homeostasis

UMMS Affiliation

Department of Cell Biology

Publication Date

2012-01-31

Document Type

Article

Subjects

MicroRNAs; Bone Development; Bone and Bones

Disciplines

Cell Biology

Abstract

MicroRNAs (miRNAs) repress cellular protein levels to provide a sophisticated parameter of gene regulation that coordinates a broad spectrum of biological processes. Bone organogenesis is a complex process involving the differentiation and crosstalk of multiple cell types for formation and remodeling of the skeleton. Inhibition of mRNA translation by miRNAs has emerged as an important regulator of developmental osteogenic signaling pathways, osteoblast growth and differentiation, osteoclast-mediated bone resorption activity and bone homeostasis in the adult skeleton. miRNAs control multiple layers of gene regulation for bone development and postnatal functions, from the initial response of stem/progenitor cells to the structural and metabolic activity of the mature tissue. This Review brings into focus an emerging concept of bone-regulating miRNAs, the evidence for which has been gathered largely from in vivo mouse models and in vitro studies in human and mouse skeletal cell populations. Characterization of miRNAs that operate through tissue-specific transcription factors in osteoblast and osteoclast lineage cells, as well as intricate feedforward and reverse loops, has provided novel insights into the supervision of signaling pathways and regulatory networks controlling normal bone formation and turnover. The current knowledge of miRNAs characteristic of human pathologic disorders of the skeleton is presented with a future goal towards translational studies.

DOI of Published Version

10.1038/nrendo.2011.234

Source

Nat Rev Endocrinol. 2012 Jan 31;8(4):212-27. doi: 10.1038/nrendo.2011.234. Link to article on publisher's site

Journal/Book/Conference Title

Nature reviews. Endocrinology

Related Resources

Link to Article in PubMed

PubMed ID

22290358

Link to Full Text

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