Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137

Yu, Yingfeng; Yao, Peiquan; Wang, Zhikun; Xie, Wenwei

doi:10.1186/s12891-020-03458-0

Cited by 14 publications

(6 citation statements)

References 27 publications

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“…AC005261.1 is antisense to a KRAB-containing zinc finger transcription gene ZNF304 , which plays a fundamental role in T-cell differentiation (Sabater et al, 2002). FTX, an X-inactive-specific transcript regulator, previously was demonstrated to have a regulatory function in cell proliferation of multiple tumor types (Huang et al, 2020), and its down-regulation promotes the differentiation of osteoclasts in osteoporosis (Yu et al, 2020b). Taken together, these results demonstrate that dynamic expression of lncRNA genes is an integral component of the transcriptional profiles of osteogenic differentiation and may contribute to the regulation of osteogenic differentiation by regulating proximal coding genes.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic landscape of human induced pluripotent stem cell-derived osteogenic differentiation identifies a regulatory role of KLF16

Ru,

Ma,

Zhou

et al. 2024

Preprint

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Osteogenic differentiation is essential for bone development and metabolism, but the underlying gene regulatory networks have not been well investigated. We differentiated mesenchymal stem cells, derived from 20 human induced pluripotent stem cell lines, into preosteoblasts and osteoblasts, and performed systematic RNA-seq analyses of 60 samples for differential gene expression. We noted a highly significant correlation in expression patterns and genomic proximity among transcription factor (TF) and long noncoding RNA (lncRNA) genes. We identified TF-TF regulatory networks, regulatory roles of lncRNAs on their neighboring coding genes for TFs and splicing factors, and differential splicing of TF, lncRNA, and splicing factor genes. TF-TF regulatory and gene co-expression network analyses suggested an inhibitory role of TF KLF16 in osteogenic differentiation. We demonstrate that in vitro overexpression of human KLF16 inhibits osteogenic differentiation and mineralization, and in vivo Klf16+/- mice exhibit increased bone mineral density, trabecular number, and cortical bone area. Thus, our model system highlights the regulatory complexity of osteogenic differentiation and identifies novel osteogenic genes.

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Section: Resultsmentioning

confidence: 99%

Transcriptomic landscape of human induced pluripotent stem cell-derived osteogenic differentiation identifies a regulatory role of KLF16

Ru,

Ma,

Zhou

et al. 2024

Preprint

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“…Some studies (17%) recruited younger participants in healthy control groups [ 38 , 41 , 42 , 44 , 47 , 59 , 60 , 71 , 78 ] and did not match for age, causing potential selection bias. Almost all the studies considered female osteoporotic and sarcopenic patients (76%), but 14/59 studies also included male patients [ 34 , 38 , 50 , 52 , 53 , 58 , 59 , 60 , 61 , 62 , 66 , 73 , 77 , 82 , 83 ]. Twelve studies on osteoporosis and two on sarcopenia did not state sex.…”

Section: Resultsmentioning

confidence: 99%

Sharing Circulating Micro-RNAs between Osteoporosis and Sarcopenia: A Systematic Review

Salamanna

Contartese

Ruffilli

et al. 2023

Life

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Background: Osteosarcopenia, a combination of osteopenia/osteoporosis and sarcopenia, is a common condition among older adults. While numerous studies and meta-analyses have been conducted on osteoporosis biomarkers, biomarker utility in osteosarcopenia still lacks evidence. Here, we carried out a systematic review to explore and analyze the potential clinical of circulating microRNAs (miRs) shared between osteoporosis/osteopenia and sarcopenia. Methods: We performed a systematic review on PubMed, Scopus, and Embase for differentially expressed miRs (p-value < 0.05) in (i) osteoporosis and (ii) sarcopenia. Following screening for title and abstract and deduplication, 83 studies on osteoporosis and 11 on sarcopenia were identified for full-text screening. Full-text screening identified 54 studies on osteoporosis, 4 on sarcopenia, and 1 on both osteoporosis and sarcopenia. Results: A total of 69 miRs were identified for osteoporosis and 14 for sarcopenia. There were 9 shared miRs, with evidence of dysregulation (up- or down-regulation), in both osteoporosis and sarcopenia: miR-23a-3p, miR-29a, miR-93, miR-133a and b, miR-155, miR-206, miR-208, miR-222, and miR-328, with functions and targets implicated in the pathogenesis of osteosarcopenia. However, there was little agreement in the results across studies and insufficient data for miRs in sarcopenia, and only three miRs, miR-155, miR-206, and miR-328, showed the same direction of dysregulation (down-regulation) in both osteoporosis and sarcopenia. Additionally, for most identified miRs there has been no replication by more than one study, and this is particularly true for all miRs analyzed in sarcopenia. The study quality was typically rated intermediate/high risk of bias. The large heterogeneity of the studies made it impossible to perform a meta-analysis. Conclusions: The findings of this review are particularly novel, as miRs have not yet been explored in the context of osteosarcopenia. The dysregulation of miRs identified in this review may provide important clues to better understand the pathogenesis of osteosarcopenia, while also laying the foundations for further studies to lead to effective screening, monitoring, or treatment strategies.

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“…MiR-137 has been reported to participate in the progression of various cancers ( Li et al , 2017 ; Liu et al , 2017; Qin et al , 2017 ; Luo et al , 2018 ; Zhang et al , 2018 ), development and maturation of neurons ( Silber et al , 2008 ; Szulwach et al , 2010 ; Tarantino et al , 2010 ; Sun et al , 2011 ; Jiang et al , 2013 ) and bone metabolism ( Zheng et al ,2019 ; Kong et al , 2020 ; Ma et al , 2020 ; Yu et al , 2020 ; Fan et al , 2021 ). But compared with the previous two research fields, miR-137-modulated osteogenic differentiation is still unclear.…”

Section: Discussionmentioning

confidence: 99%

“…It has been demonstrated that miR-137 acts as a key regulator in various kinds of malignancies ( Li et al , 2017 ; Liu et al , 2017 ; Qin et al , 2017 ; Luo et al , 2018 ; Zhang et al , 2018 ) and neural development ( Silber et al , 2008 ; Szulwach et al , 2010 ; Tarantino et al , 2010 ; Sun et al , 2011 ; Jiang et al ,2013 ). But up to present, only a few studies investigated the effects of miR-137 on osteogenesis ( Zheng et al , 2019 ; Kong et al , 2020 ; Ma et al , 2020 ; Yu et al , 2020 ; Fan et al , 2021 ), and the mechanisms of osteogenic modulation by miR-137 are still not fully understood, especially considering the diverse biological properties of different cell types.…”

Section: Introductionmentioning

confidence: 99%

MiR-137-mediated negative relationship between LGR4 and RANKL modulated osteogenic differentiation of human adipose-derived mesenchymal stem cells

Fan

2022

Genet. Mol. Biol.

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has recently emerged as an osteogenic regulator in several cell lines. This study aimed to identify the function of miR-137 on the crosstalk between leucine rich repeat containing G protein-coupled receptor 4 (LGR4) and receptor activator of nuclear factor-κB ligand (RANKL), thus unveiling the critical role of LGR4-RANKL interplay in the osteogenic differentiation of human adipose-derived mesenchymal stem cells (hASCs). By examining the osteogenic capacity and possible downstream genes expression with miR-137 overexpression/knockdown, we found that miR-137 downregulated LGR4 while upregulating RANKL. According to the results of dual-luciferase reporter assay, LGR4 was validated as a direct target of miR-137. Surprisingly, a negative relationship between LGR4 and RANKL was confirmed by the knockdown of these two genes. Furthermore, RANKL inhibitor could alleviate or reverse the inhibitory effects on osteogenesis generated by LGR4 knockdown. Collectively, this study indicated that miR-137-induced a negative crosstalk between LGR4 and RANKL that could contribute to the osteogenic regulation of hASCs and provide more systematic and in-depth understanding of epigenetic modulation by miR-137.

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Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137

Cited by 14 publications

References 27 publications

Transcriptomic landscape of human induced pluripotent stem cell-derived osteogenic differentiation identifies a regulatory role of KLF16

Transcriptomic landscape of human induced pluripotent stem cell-derived osteogenic differentiation identifies a regulatory role of KLF16

Sharing Circulating Micro-RNAs between Osteoporosis and Sarcopenia: A Systematic Review

MiR-137-mediated negative relationship between LGR4 and RANKL modulated osteogenic differentiation of human adipose-derived mesenchymal stem cells

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