miR-218 is involved in the negative regulation of osteoclastogenesis and bone resorption by partial suppression of p38MAPK-c-Fos-NFATc1 signaling: Potential role for osteopenic diseases

Qu, Bo; Xia, Xun; Yan, Ming; Gong, Kai; Deng, Song; Huang, Gang; Ma, Zehui; Pan, Xian-Ming

doi:10.1016/j.yexcr.2015.07.023

Cited by 31 publications

(28 citation statements)

References 30 publications

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“…While miR-7b was down-regulated during osteoclastogenesis in RAW264.7 cells stimulated by M-CSF and RANKL, and overexpression of miR-7b decreased TRAP-positive MNCs in number, inhibition of miR-7b promoted osteoclastogenesis [28]. Besides, Qu et al [29] manifested that miR-218-5p acted as a negative regulator of osteoclastogenesis by targeting the p38MAPK-c-Fos-NFATc1 pathway. Chen et al [30] also presented that miR-503 inhibited osteoclast differentiation by suppressing RANK, which was a target of miR-503.…”

Section: Discussionmentioning

confidence: 99%

miRNA-340 inhibits osteoclast differentiation via repression of MITF

et al. 2017

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Many miRNAs play critical roles in modulating various biological processes of osteoclast differentiation and function. Microphthalmia-associated transcription factor (MITF), a target of miR-340, served as pivotal transcription factor involved in osteoclast differentiation. However, the role of miR-340 and MITF during osteoclast differentiation has not yet been clearly established. Tartrate-resistant acid phosphatase (TRAP) staining assay was performed to identify osteoclasts differentiated from bone marrow-derived macrophages (BMMs). Quantitative reverse transcription PCR (qRT-PCR) or Western blotting was undertaken to examine the mRNA or protein expression respectively. Luciferase reporter assay was performed to investigate the interaction between miR-340 and MITF. MITF was knocked down and miR-340 was overexpressed and transfected into BMMs to detect their effects on osteoclast differentiation. Firstly, qRT-PCR analysis showed that miR-340 was down-regulated during osteoclast differentiation stimulated by macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor (NF)-κB (RANK) ligand (RANKL). Besides, we found that overexpression of miRNA-340 inhibited osteoclast differentiation and suppressed both the mRNA and protein level of MITF. Finally, Western blot and qRT-PCR analysis revealed that silencing MITF inhibited TRAP, calcitonin receptor, V-ATPase d2, and cathepsin K. miR-340 suppresses osteoclast differentiation by inhibiting MITF. Our findings may provide promising therapeutic targets for osteoclast-associated diseases.

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Section: Discussionmentioning

confidence: 99%

miRNA-340 inhibits osteoclast differentiation via repression of MITF

et al. 2017

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“…Osteoclasts play a vital role in the periodontitis pathological bone loss and physiological bone remodelling. MiR‐218 has been reported to decrease during osteoclastogenesis induced by RANKL (Qu et al, ). We next investigated the effect of miR‐218 on osteoclastogenesis.…”

Section: Resultsmentioning

confidence: 99%

“…Kabsun Kim found that miR‐26a negatively regulates the osteoclast production induced by RANKL through repressing CTGF expression (Kim et al, ). MiR‐183 can increase RANKL‐induced osteoclastogenesis through suppressing haem oxygenase‐1 expression (Ke, Sul, Rajasekaran, & Choi, ), although miR‐218 involved in the negative regulation of osteoblast differentiation and bone resorption has been reported (Qu et al, ). This study first demonstrated that miR‐218 could attenuate the osteoclast formation by regulating Mmp9 expression.…”

Section: Discussionmentioning

confidence: 99%

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Expression of Concern: MiRNA‐218 regulates osteoclast differentiation and inflammation response in periodontitis rats through Mmp9

Guo

Zeng

Miao

et al. 2019

Cellular Microbiology

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Periodontitis is a multiple infection and inflammatory disease featured by connective tissue homeostasis loss, periodontal inflammation, and alveolar bone resorption. MicroRNAs (miRNAs) are involved in the mediation of a large scale of pathological processes. Here, we show that miRNA‐218 provides protective effect on periodontitis via regulation of matrix metalloproteinase‐9 (Mmp9). This pathway is aberrant in periodontium from rats with periodontitis and human periodontal ligament progenitor cells stimulated by lipopolysaccharide, with downregulation of miR‐218 and higher levels of Mmp9 compared with periodontium from healthy rats and cells without stimulation. Overexpression of miR‐218 can suppress the degradation of Collagen Types I and IV and dentin sialoprotein (DSP), attenuate osteoclast formation, and inhibit the secretion of proinflammatory cytokines. On the other hand, overexpression of Mmp9 promotes the degradation of Collagen Types I and IV and DSP as well as RANKL‐induced osteoclast formation and elevates inflammatory factors levels. Furthermore, the inhibitory effect of miR‐218 was prevented by rescuing the Mmp9 expression. In addition, we also have showed that miR‐218 was able to attenuate bone resorption and inflammation in a periodontitis rat model. Collectively, our findings therefore suggest that miR‐218 acts as a protective role in periodontitis through the regulation of Mmp9.

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“…For example, miR-29 (Franceschetti et al, 2013), miR-31-5p (Mizoguchi et al, 2013), miR-183-5p (Ke et al, 2015), and miR-214 (Zhao et al, 2015) have been reported to be upregulated in BMMs and promote osteoclast formation. In contrast, miR-7b-5p (Dou et al, 2014), miR-34a-5p (Krzeszinski et al, 2014), miR-124-3p (Lee et al, 2013), and miR-218-5p (Qu et al, 2015) were downregulated in BMMs and inhibited osteoclast formation. However, the relationship between the expression pattern of miRNA and its role in osteoclastogenesis is complex.…”

Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor β1/Smad4 Signaling Affects Osteoclast Differentiation via Regulation of miR-155 Expression

Zhao

Zhang

Shao

et al. 2017

Molecules and Cells

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Transforming growth factor β1 (TGFβ1)/Smad4 signaling plays a pivotal role in maintenance of the dynamic balance between bone formation and resorption. The microRNA miR-155 has been reported to exert a significant role in the differentiation of macrophage and dendritic cells. The goal of this study was to determine whether miR-155 regulates osteoclast differentiation through TGFβ1/Smad4 signaling. Here, we present that TGFβ1 elevated miR-155 levels during osteoclast differentiation through the stimulation of M-CSF and RANKL. Additionally, we found that silencing Smad4 attenuated the upregulation of miR-155 induced by TGFβ1. The results of luciferase reporter experiments and ChIP assays demonstrated that TGFβ1 promoted the binding of Smad4 to the miR-155 promoter at a site located in 454 bp from the transcription start site in vivo, further verifying that miR-155 is a transcriptional target of the TGFβ1/Smad4 pathway. Subsequently, TRAP staining and qRT-PCR analysis revealed that silencing Smad4 impaired the TGFβ1-mediated inhibition on osteoclast differentiation. Finally, we found that miR-155 may target SOCS1 and MITF to suppress osteoclast differentiation. Taken together, we provide the first evidence that TGFβ1/Smad4 signaling affects osteoclast differentiation by regulation of miR-155 expression and the use of miR-155 as a potential therapeutic target for osteoclast-related diseases shows great promise.

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miR-218 is involved in the negative regulation of osteoclastogenesis and bone resorption by partial suppression of p38MAPK-c-Fos-NFATc1 signaling: Potential role for osteopenic diseases

Cited by 31 publications

References 30 publications

miRNA-340 inhibits osteoclast differentiation via repression of MITF

miRNA-340 inhibits osteoclast differentiation via repression of MITF

Expression of Concern: MiRNA‐218 regulates osteoclast differentiation and inflammation response in periodontitis rats through Mmp9

Transforming Growth Factor β1/Smad4 Signaling Affects Osteoclast Differentiation via Regulation of miR-155 Expression

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