miR-23a/b regulates the balance between osteoblast and adipocyte differentiation in bone marrow mesenchymal stem cells

Guo, Qi; Chen, Yusi; Guo, Lijuan; Tong, Jiang; Lin, Zhenghua

doi:10.1038/boneres.2016.22

Cited by 55 publications

(54 citation statements)

References 32 publications

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“…Bone homeostasis is maintained by the balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. 13,14 In the present study, we investigated the role of GDF8 in bone formation in vitro and in vivo, and showed that GDF8 inhibited mouse osteoblast differentiation and repressed bone formation in vivo. Accumulated data demonstrate that GDF8 plays an inhibitory role in controlling bone mass.…”

Section: Discussionmentioning

confidence: 86%

GDF8 inhibits bone formation and promotes bone resorption in mice

Chen

Guo

et al. 2017

Clin Exp Pharma Physio

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Growth Differentiation Factor 8 (GDF8), also called myostatin, is a member of the transforming growth factor (TGF)-β super-family. As a negative regulator of skeletal muscle growth, GDF8 is also associated with bone metabolism. However, the function of GDF8 in bone metabolism is not fully understood. Our study aimed to investigate the role of GDF8 in bone metabolism, both in vitro and in vivo. Our results showed that GDF8 had a negative regulatory effect on primary mouse osteoblasts, and promoted receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis in vitro. Intraperitoneal injection of recombinant GDF8 repressed bone formation and accelerated bone resorption in mice. Furthermore, treatment of aged mice with a GDF8 neutralizing antibody stimulated new bone formation and prevented bone resorption. Thus, our study showed that GDF8 plays a significant regulatory role in bone formation and bone resorption, thus providing a potential therapeutic pathway for osteoporosis.

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Section: Discussionmentioning

confidence: 86%

GDF8 inhibits bone formation and promotes bone resorption in mice

Chen

Guo

et al. 2017

Clin Exp Pharma Physio

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“…Aging in bone tissue is characterized by decreased bone formation and increased bone resorption, often leading to diseases such as osteoporosis (Guo, Chen, Guo, Jiang, & Lin, 2016; Wu et al., 2017). The balance between bone formation by osteoblasts and bone resorption by osteoclasts is important to maintain bone mass.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐31a‐5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment

et al. 2018

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The alteration of age‐related molecules in the bone marrow microenvironment is one of the driving forces in osteoporosis. These molecules inhibit bone formation and promote bone resorption by regulating osteoblastic and osteoclastic activity, contributing to age‐related bone loss. Here, we observed that the level of microRNA‐31a‐5p (miR‐31a‐5p) was significantly increased in bone marrow stromal cells (BMSCs) from aged rats, and these BMSCs demonstrated increased adipogenesis and aging phenotypes as well as decreased osteogenesis and stemness. We used the gain‐of‐function and knockdown approach to delineate the roles of miR‐31a‐5p in osteogenic differentiation by assessing the decrease of special AT‐rich sequence‐binding protein 2 (SATB2) levels and the aging of BMSCs by regulating the decline of E2F2 and recruiting senescence‐associated heterochromatin foci (SAHF). Notably, expression of miR‐31a‐5p, which promotes osteoclastogenesis and bone resorption, was markedly higher in BMSCs‐derived exosomes from aged rats compared to those from young rats, and suppression of exosomal miR‐31a‐5p inhibited the differentiation and function of osteoclasts, as shown by elevated RhoA activity. Moreover, using antagomiR‐31a‐5p, we observed that, in the bone marrow microenvironment, inhibition of miR‐31a‐5p prevented bone loss and decreased the osteoclastic activity of aged rats. Collectively, our results reveal that miR‐31a‐5p acts as a key modulator in the age‐related bone marrow microenvironment by influencing osteoblastic and osteoclastic differentiation and that it may be a potential therapeutic target for age‐related osteoporosis.

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“…In vitro study on human bone marrow mesenchymal stem cells (hBMSCs) revealed that increased miR‐23a/b expression could promote osteoblastic differentiation . Moreover, it was further shown in vivo that continuous stimulation on differentiation could eventually lead to bone mass reduction, where increased level of miR‐23a in osteoblast could promote its terminal differentiation to osteocyte .…”

Section: Mirnas In Human Osteoporosis Studiesmentioning

confidence: 99%

MicroRNA and Human Bone Health

Cheng

Tan

et al. 2018

JBMR Plus

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The small non‐coding microRNAs (miRNAs) are post‐transcription regulators that modulate diverse cellular process in bone cells. Because optimal miRNA targeting is essential for their function, single‐nucleotide polymorphisms (SNPs) within or proximal to the loci of miRNA (miR‐SNPs) or mRNA (PolymiRTS) could potentially disrupt the miRNA‐mRNA interaction, leading to changes in bone metabolism and osteoporosis. Recent human studies of skeletal traits using miRNA profiling, genomewide association studies, and functional studies started to decipher the complex miRNA regulatory network. These studies have indicated that miRNAs may be a promising bone marker. This review focuses on human miRNA studies on bone traits and discusses how genetic variants affect bone metabolic pathways. Major ex vivo investigations using human samples supported with animal and in vitro models have shed light on the mechanistic role of miRNAs. Furthermore, studying the miRNAs’ signatures in secondary osteoporosis and osteoporotic medications such as teriparatide (TPTD) and denosumab (DMab) have provided valuable insight into clinical management of the disease. © 2018 The Authors. JBMR Plus Published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research

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miR-23a/b regulates the balance between osteoblast and adipocyte differentiation in bone marrow mesenchymal stem cells

Cited by 55 publications

References 32 publications

GDF8 inhibits bone formation and promotes bone resorption in mice

GDF8 inhibits bone formation and promotes bone resorption in mice

MicroRNA‐31a‐5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment

MicroRNA and Human Bone Health

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