25-hydroxycholesterol promotes RANKL-induced osteoclastogenesis through coordinating NFATc1 and Sp1 complex in the transcription of miR-139-5p

Zhang, Lishan; Lv, Yinping; Xian, Guozhe; Lin, Yen‐Ting

doi:10.1016/j.bbrc.2017.02.118

Cited by 17 publications

(16 citation statements)

References 26 publications

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“…SP1 is an important transcription factor in the process of osteogenic/osteoclast differentiation and can promote the expression of different factors in the process of bone differentiation, such as RANKL (Liu et al 2005 ), miR-139-5p (Zhang et al 2017 ), miR-545-3p (Li et al 2019 ), Frizzled-1 (Yu et al 2016 ). However, reports on the function of SP1 in osteogenesis/osteoclast differentiation is not completely consistent, which might be related to the transcriptional regulation of genes.…”

Section: Discussionmentioning

confidence: 99%

lncRNA SNHG1 induced by SP1 regulates bone remodeling and angiogenesis via sponging miR-181c-5p and modulating SFRP1/Wnt signaling pathway

Rong

Song

et al. 2021

Mol Med

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Background We aimed to investigate the functions and underlying mechanism of lncRNA SNHG1 in bone differentiation and angiogenesis in the development of osteoporosis. Methods The differential gene or proteins expressions were measured by qPCR or western blot assays, respectively. The targeted relationships among molecular were confirmed through luciferase reporter, RIP and ChIP assays, respectively. Alkaline phosphatase (ALP), alizarin red S (ARS) and TRAP staining were performed to measure the osteoblast/osteoclast differentiation of BMSCs. The viability, migration and angiogenesis in BM-EPCs were validated by CCK-8, clone formation, transwell and tube formation assays, respectively. Western blot and immunofluorescence detected the cytosolic/nuclear localization of β-catenin. Ovariectomized (OVX) mice were established to confirm the findings in vitro. Results SNHG1 was enhanced and miR-181c-5p was decreased in serum and femoral tissue from OVX mice. SNHG1 directly inhibited miR-181c-5p to activate Wnt3a/β-catenin signaling by upregulating SFRP1. In addition, knockdown of SNHG1 promoted the osteogenic differentiation of BMSCs by increasing miR-181c-5p. In contrast, SNHG1 overexpression advanced the osteoclast differentiation of BMSCs and inhibited the angiogenesis of BM-EPCs, whereas these effects were all reversed by miR-181c-5p overexpression. In vivo experiments indicated that SNHG1 silencing alleviated osteoporosis through stimulating osteoblastogenesis and inhibiting osteoclastogenesis by modulating miR-181c-5p. Importantly, SNHG1 could be induced by SP1 in BMSCs. Conclusions Collectively, SP1-induced SNHG1 modulated SFRP1/Wnt/β-catenin signaling pathway via sponging miR-181c-5p, thereby inhibiting osteoblast differentiation and angiogenesis while promoting osteoclast formation. Further, SNHG1 silence might provide a potential treatment for osteoporosis. Graphic abstract

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Section: Discussionmentioning

confidence: 99%

lncRNA SNHG1 induced by SP1 regulates bone remodeling and angiogenesis via sponging miR-181c-5p and modulating SFRP1/Wnt signaling pathway

Rong

Song

et al. 2021

Mol Med

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“…After exposure of RAW264.7 cells to CM, the expression of miR-139 was inhibited and c-Fos expression was increased, which was enhanced by 27-HC treatment. Our previous result indicates that miR-139 overexpression impairs RANKL-induced osteoclast differentiation (Zhang et al, 2017), suggesting that CM might facilitate osteoclast differentiation from RAW264.7. As expected, Koarai et al, 2012;Lavin et al, 2017), among of which TNF-α and IL-8 have been demonstrated as stimulator of osteoclastogenesis (Bendre et al, 2005;Courbon et al, 2017).…”

Section: Discussionmentioning

confidence: 92%

27‐Hydroxycholesterol enhanced osteoclastogenesis in lung adenocarcinoma microenvironment

Zhang

Liu

et al. 2018

Journal Cellular Physiology

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27‐Hydroxycholesterol (27‐HC) has been implicated in the pathological process of estrogen receptor positive breast cancer. However, the role of 27‐HC in lung adenocarcinoma is still unclear. Because bone metastasis is a main reason for the high mortality of lung adenocarcinoma, this study aimed to investigate the effect of 27‐HC on osteoclastogenesis in lung adenocarcinoma microenvironment. The results showed that the conditioned media (CM) from lung adenocarcinoma cells cocultured with macrophages promoted osteoclast differentiation, which was enhanced by 27‐HC. Further investigation showed that CM inhibited miR‐139 expression and promoted c‐Fos expression. Luciferase reporter assay identified c‐Fos as a direct target of miR‐139. CM also induced the expression and nuclear translocation of NFATc1 and STAT3 phosphorylation, which was enlarged by 27‐HC but was attenuated by miR‐139. Coimmunoprecipitation assay demonstrated that 27‐HC increased the interaction between NFATc1 and phosphorylated STAT3, which was restricted by miR‐139. Chromatin immunoprecipitation assay showed that pSTAT3 could bind to the promoter of c‐Fos, c‐Fos could bind to the promoter of NFATc1, and both pSTAT3 and NFATc1 could bind to the promoter of Oscar, which were enlarged by 27‐HC but were blocked by miR‐139. Knockdown of c‐Fos mimicked the effect of miR‐139. These results suggested that CM, especially containing 27‐HC, promoted osteoclastogenesis by inhibiting miR‐139 expression and activating the STAT3/c‐Fos/NFATc1 pathway.

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“…Our findings support that over-expression of microRNA-139-5p reduced cell proliferation, increased LDH activity level and caspase-3/9 activity levels, and inhibited Col I, ALP, BMP2, osteopontin and osteocalcin mRNA expressions in BMSCs. Zhang et al suggested that 25-hydroxycholesterol promotes RANKL-induced osteoclastogenesis through miR-139-5p [20].…”

Section: Discussionmentioning

confidence: 99%

The Inhibition of MicroRNA-139-5p Promoted Osteoporosis of Bone Marrow-Derived Mesenchymal Stem Cells by Targeting Wnt/Beta- Catenin Signaling Pathway by NOTCH1

Feng¹,

Wan²,

Yin³

et al. 2020

Journal of Microbiology and Biotechnology

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We investigated the therapeutic effects of microRNA-139-5p in relation to osteoporosis of bone marrow-derived mesenchymal stem cell (BMSCs) and its underlying mechanisms. In this study we used a dexamethasone-induced in vivo model of osteoporosis and BMSCs were used for the in vitro model. Real-time quantitative polymerase chain reaction (RT-PCR) and gene chip were used to analyze the expression of microRNA-139-5p. In an osteoporosis rat model, the expression of microRNA-139-5p was increased, compared with normal group. Downregulation of microRNA-139-5p promotes cell proliferation and osteogenic differentiation in BMSCs. Especially, up-regulation of microRNA-139-5p reduced cell proliferation and osteogenic differentiation in BMSCs. Overexpression of miR-139-5p induced Wnt/β-catenin and down-regulated NOTCH1 signaling in BMSCs. Down-regulation of miR-139-5p suppressed Wnt/β-catenin and induced NOTCH1 signaling in BMSCs. The inhibition of NOTCH1 reduced the effects of anti-miR-139-5p on cell proliferation and osteogenic differentiation in BMSCs. Activation of Wnt/β-catenin also inhibited the effects of anti-miR-139-5p on cell proliferation and osteogenic differentiation in BMSCs. Taken together, our results suggested that the inhibition of microRNA-139-5p promotes osteogenic differentiation of BMSCs via targeting Wnt/β-catenin signaling pathway by NOTCH1.

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25-hydroxycholesterol promotes RANKL-induced osteoclastogenesis through coordinating NFATc1 and Sp1 complex in the transcription of miR-139-5p

Cited by 17 publications

References 26 publications

lncRNA SNHG1 induced by SP1 regulates bone remodeling and angiogenesis via sponging miR-181c-5p and modulating SFRP1/Wnt signaling pathway

lncRNA SNHG1 induced by SP1 regulates bone remodeling and angiogenesis via sponging miR-181c-5p and modulating SFRP1/Wnt signaling pathway

27‐Hydroxycholesterol enhanced osteoclastogenesis in lung adenocarcinoma microenvironment

The Inhibition of MicroRNA-139-5p Promoted Osteoporosis of Bone Marrow-Derived Mesenchymal Stem Cells by Targeting Wnt/Beta- Catenin Signaling Pathway by NOTCH1

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