Abstract
MicroRNAs (miRNAs) have been widely demonstrated to interact with multiple cellular signaling pathways and to participate in a wide range of physiological processes. Estradiol-17β (E2) is the most potent and prevalent endogenous estrogen that plays a vital role in promoting bone formation and reducing bone resorption. Currently, little is known about the regulation of miRNAs in E2-induced osteogenic differentiation. In the present study, the primary bone marrow mesenchymal stem cells from rats (rBMSCs) were isolated and incubated with E2, followed by miRNA profiling. The microarray showed that 29 miRNAs were differentially expressed in response to E2 stimulation. Further verification by real-time reverse-transcriptase polymerase chain reaction revealed that E2 enhanced the expression of let-7b and miR-25 but suppressed the miR-30b expression. Moreover, a gain-of-function experiment confirmed that miR-30b negatively regulated the E2-induced osteogenic differentiation. These data suggest an important role of miRNAs in osteogenic differentiation.
Highlights
Osteoporosis is a global public health problem and potentially causes serious fractures, disability, and chronic pain, leading to financial burdens for families and lower quality of life for individuals
To investigate the osteogenic differentiation potential, Rat Bone Marrow Mesenchymal Stem Cells (rBMSCs) were exposed to the osteogenic differentiation medium (OM), which is complete medium (CM) supplemented with 10 nM dexamethasone
Our study revealed the miRNA expression profile during estrogen-promoted osteogenic differentiation and explored the role of miR-30b in this process, indicating that miRNA-targeted treatment could be a new strategy for osteoporosis therapy
Summary
Osteoporosis is a global public health problem and potentially causes serious fractures, disability, and chronic pain, leading to financial burdens for families and lower quality of life for individuals. Bone remodeling is a process that relies on the dynamic equilibrium between osteoclasts and osteoblasts. It has been well established by both in vivo and in vitro studies that estrogen inhibits osteoclast formation [2]. Several studies suggested that estrogen could inhibit osteoblast apoptosis and promote osteoblast differentiation, protecting against bone loss [6, 7]. Estradiol-17β (E2) is the most potent estrogen that could effectively improve bone mesenchymal stem cell (BMSC) proliferation and osteogenic differentiation in various species, including mouse, rat, and human [8,9,10]. According to its ability to improve bone mineral density and reduce fracture incidence, estrogen replacement therapy is a conventional way to treat osteoporosis. Investigating the molecular mechanisms of estrogen-induced osteoblastic differentiation is
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