Identification of differentially expressed microRNAs involved in non-traumatic osteonecrosis through microRNA expression profiling

Wu, Xing-Jing; Zhang, Yongtao; Guo, Xiong; Xu, Huazi; Xu, Zhujun; Duan, Dapeng; Wang, Kunzheng

doi:10.1016/j.gene.2015.03.072

Cited by 37 publications

(33 citation statements)

References 33 publications

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“…In addition, the expression of VKORC1 mRNA (Fig. 2E) was inversely correlated with miR-133a expression, as previously reported (14), increasing 13-fold in osteogenic-induced hBMSCs at day 14. These results suggested that the osteogenic differentiation of BMSCs was associated with a reduction in miR-133a expression levels, indicating that miR-133a may be associated with the osteoblast differentiation of mesenchymal cells.…”

Section: Resultssupporting

confidence: 87%

“…Studies have demonstrated the expression of miR-133a in mesenchymal stem cells, where it acts as a negative regulator of osteoblast differentiation (10–12). Furthermore, Wang et al (13) suggested that miR-133a expression levels in circulating monocytes were upregulated in patients with osteoporosis and Wu et al (14) discovered that mir-133a was significantly downregulated in non-traumatic osteonecrosis of the femoral head samples compared with femoral neck fracture samples, indicating that miR-133a may be a key regulator of bone metabolism.…”

Section: Introductionmentioning

confidence: 99%

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Vitamin K2 promotes mesenchymal stem cell differentiation by inhibiting miR-133a expression

Zhang

Weng

Yin

et al. 2017

Molecular Medicine Reports

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Vitamin K2 has been demonstrated to promote the osteogenic differentiation of mesenchymal stem cells; however, the mechanisms underlying this effect remain unclear. As microRNA (miR)-133a has been identified as a negative regulator of osteogenic differentiation, the present study hypothesized that vitamin K2 promoted osteogenesis by inhibiting miR-133a. Using human bone marrow stromal cells (hBMSCs) overexpressing miR-133a, or a control, the expression levels of osteogenesis-associated proteins, including runt-related transcription factor 2, alkaline phosphatase and osteocalcin, were analyzed. miR-133a significantly suppressed the osteogenic differentiation of hBMSCs. To determine the effect of vitamin K2 on miR-133a expression and osteogenesis, hBMSCs were treated with vitamin K2. Vitamin K2 inhibited miR-133a expression, which was accompanied by enhanced osteogenic differentiation. Furthermore, the expression levels of vitamin K epoxide reductase complex subunit 1, the key protein in γ-carboxylation, were downregulated by miR-133a overexpression and upregulated by vitamin K2 treatment, indicating a positive feedback on γ-carboxylation. The results of the present study suggested that vitamin K2 targets miR-133a to regulate osteogenesis.

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Section: Resultssupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Vitamin K2 promotes mesenchymal stem cell differentiation by inhibiting miR-133a expression

Zhang

Weng

Yin

et al. 2017

Molecular Medicine Reports

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“…In particular, miRNAs such as miR-31, miR-34c, and miR-338–3p have been shown to be involved in regulating BMSC differentiation272829. Moreover, altered miRNA expression has been identified in ONFH and other bone necrosis diseases3031. Therefore, it is important to identify specific miRNAs and their targets that are involved in BMSC fate regulation and investigate the detailed mechanisms of steroid-induced ONFH to shed light on the disease pathogenesis and develop novel and effective therapeutic approaches.…”

Section: Discussionmentioning

confidence: 99%

miR-27a attenuates adipogenesis and promotes osteogenesis in steroid-induced rat BMSCs by targeting PPARγ and GREM1

Zhang

et al. 2016

Sci Rep

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The imbalance between adipogenic and osteogenic differentiation in bone marrow mesenchymal stem cells (BMSCs) plays a significant role in the pathogenesis of steroid-induced osteonecrosis of the femoral head (ONFH). Several microRNAs (miRNAs) are involved in regulating adipogenesis and osteogenesis. In this study, we established a steroid-induced ONFH rat model to identify the potential relevant miRNAs. We identified 9 up-regulated and 28 down-regulated miRNAs in the ONFH rat model. Of these, miR-27a was down-regulated and negatively correlated with peroxisome proliferator-activated receptor gamma (PPARγ) and gremlin 1 (GREM1) expression. Further studies confirmed that PPARγ and GREM1 were direct targets of miRNA-27a. Additionally, adipogenic differentiation was enhanced by miR-27a down-regulation, whereas miRNA-27a up-regulation attenuated adipogenesis and promoted osteogenesis in steroid-induced rat BMSCs. Moreover, miRNA-27a up-regulation had a stronger effect on adipogenic and osteogenic differentiation in steroid-induced rat BMSCs than si-PPARγ and si-GREM1. In conclusion, we identified 37 differentially expressed miRNAs in the steroid-induced ONFH model, of which miR-27a was down-regulated. Our results showed that miR-27a up-regulation could inhibit adipogenesis and promote osteogenesis by directly targeting PPARγ and GREM1. Thus, miR-27a is likely a key regulator of adipogenesis in steroid-induced BMSCs and a potential therapeutic target for ONFH treatment.

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“…8,[31][32][33][34] In this study, we performed miRNA microarray to identify the differentially abundant miRNAs in the serums of SLE patients with steroidinduced ONFH as compared with SLE control and healthy control groups. Our data indicated that miR-4440 was commonly increased,…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNA signature of steroid‐induced osteonecrosis of the femoral head

Zheng

Jiang

et al. 2017

Cell Proliferation

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ObjectivesSteroid‐induced osteonecrosis of the femoral head (ONFH) is a common orthopaedic disease of which early detection remains clinically challenging. Accumulating evidences indicated that circulating microRNAs (miRNAs) plays vital roles in the development of several bone diseases. However, the association between circulating miRNAs and steroid‐induced ONFH remains elusive.Materials and methodsmiRNA microarray was performed to identify the differentially abundant miRNAs in the serums of systemic lupus erythematosus (SLE) patients with steroid‐induced ONFH as compared with SLE control and healthy control group. We predicted the potential functions of these differentially abundant miRNAs using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses and reconstructed the regulatory networks of miRNA‐mRNA interactions.ResultsOur data indicated that there were 11 differentially abundant miRNAs (2 upregulated and 9 downregulated) between SLE‐ONFH group and healthy control group and 42 differentially abundant miRNAs (14 upregulated and 28 downregulated) between SLE‐ONFH group and SLE control group. We also predicted the potential functions of these differentially abundant miRNAs using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses and reconstructed the regulatory networks of miRNA‐mRNA interactions.ConclusionsThese findings corroborated the idea that circulating miRNAs play significant roles in the development of ONFH and may serve as diagnostic markers and therapeutic targets.

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Identification of differentially expressed microRNAs involved in non-traumatic osteonecrosis through microRNA expression profiling

Cited by 37 publications

References 33 publications

Vitamin K2 promotes mesenchymal stem cell differentiation by inhibiting miR-133a expression

Vitamin K2 promotes mesenchymal stem cell differentiation by inhibiting miR-133a expression

miR-27a attenuates adipogenesis and promotes osteogenesis in steroid-induced rat BMSCs by targeting PPARγ and GREM1

Circulating microRNA signature of steroid‐induced osteonecrosis of the femoral head

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