Interferon‐β‐induced miR‐155 inhibits osteoclast differentiation by targeting SOCS1 and MITF

Zhang, Jun; Zhao, Hongying; Chen, Jinping; Xia, Bing; Jin, Yongming; Wei, Wei; Shen, Jianjian; Huang, Yanlei

doi:10.1016/j.febslet.2012.06.047

Cited by 111 publications

(84 citation statements)

References 43 publications

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“…Previously, it was shown that miR-155 was able to affect the levels of expression of other miRNAs (5), which may explain the observed effect in vivo. Such a role was already suggested for miR-155 in a previous study (36), where this miRNA was described as having modulated osteoclastogenesis by targeting SOCS1 and MITF. Interestingly, our in vivo model showed that the reduction of TNF-␣ by miR-155 was not enough to significantly decrease ICI, bone loss, or osteoclast activity.…”

Section: Gingivalis (Pg) (A To C) Combination (P Gingivalis and Mirsupporting

confidence: 59%

Identification and Characterization of MicroRNA Differentially Expressed in Macrophages Exposed to Porphyromonas gingivalis Infection

et al. 2017

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MicroRNAs (miRNAs) are short, noncoding RNAs involved in the regulation of several processes associated with inflammatory diseases and infection. Bacterial infection modulates miRNA expression to subvert any innate immune response. In this study we analyzed, using microarray analysis, the bacterial modulation of miRNAs in bone marrow-derived macrophages (BMMs) in which activity was induced by infection with Porphyromonas gingivalis. The expression of several miRNAs was modulated 3 h postinfection (at a multiplicity of infection of 25). A bioinformatic analysis was performed to further identify pathways related to the innate immune host response under the influence of selected miRNAs. To assess the effects of the miRNAs identified on cytokine secretion (tumor necrosis factor alpha [TNF-␣] and interleukin-10 [IL-10]), BMMs were transfected with selected miRNA mimics and inhibitors. Transfection with mmu-miR-155 and mmumiR-2137 did not modify TNF-␣ secretion, while their inhibitors increased it. Inhibitors of mmu-miR-2137 and mmu-miR-7674 increased the secretion of the anti-inflammatory factor IL-10. In P. gingivalis-infected BMMs, mmu-miR-155-5p significantly decreased TNF-␣ secretion while inhibitor of mmu-miR-2137 increased IL-10 secretion. In vivo, in a mouse model of P. gingivalis-induced calvarial bone resorption, injection of mmu-miR-155-5p or anti-mmu-miR-2137 reduced the size of the lesion significantly. Furthermore, anti-mmu-miR-2137 significantly reduced inflammatory cell infiltration, osteoclast activity, and bone loss. Bioinformatic analysis demonstrated that pathways related to cytokine-and chemokinerelated pathways but also osteoclast differentiation may be involved in the effects observed. This study contributes further to our understanding of P. gingivalis-induced modulation of miRNAs and their physiological effects. It highlights the potential therapeutic merits of targeting mmu-miR-155-5p and mmumiR-2137 to control inflammation induced by P. gingivalis infection.

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Section: Gingivalis (Pg) (A To C) Combination (P Gingivalis and Mirsupporting

confidence: 59%

Identification and Characterization of MicroRNA Differentially Expressed in Macrophages Exposed to Porphyromonas gingivalis Infection

et al. 2017

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“…76 Zhang et al reported that IFN-b induced miR-155 and mediated IFN-b-induced suppression of osteoclast differentiation by interacting with MITF and SOCS1, positive regulators of osteoclastogenesis. 77 Taken together, these findings demonstrate that miR-155 regulates osteoclastogenesis via targeting several essential transcriptional factors.…”

Section: Mir-155mentioning

confidence: 74%

The role of MicroRNAs in Osteoclasts and Osteoporosis

et al. 2014

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These authors contributed equally to this work. Keywords: MicroRNA, osteoclast, osteoporosisAbbreviations: GM-CSF, Granulocyte macrophage colony-stimulating factor; MiRNA, microRNA; 3'-UTR; 3' untranslated region; BMMs, bone marrow macrophages; PDCD4, programmed cell death 4; FasL, Fas ligand; PIO, particle-induced osteolysis; Calcr, calcitonin receptor; RDX, radixin; M-RIP, myosin phosphatase-Rho interacting protein; ITGA5, integrin a5; Fzd3, frizzled 3; ALP, alkaline phosphatase; TRAP, tartrate-resistant acid phosphatase; CXCL11, chemokine (C-X-C motif) ligand 11; CXCR3, chemokine (C-X-C motif) receptor 3; SLC39A1, solute carrier family (zinc transporter) member 1; TRAF6, TNF receptor-associated factor 6; OVX, ovariectomy; MAFB, V-maf musculoaponeurotic fibrosarcoma oncogene homolog B; CBL, Casitas B-lineage lymphoma proto-oncogene; PAG1, phosphoprotein associated with glycosphingolipid microdomains; TOB2, transducer of ERBB2; sICAM1, soluble intracellular adhesion molecule.Osteoclasts are the exclusive cells of bone resorption. Abnormally activating osteoclasts can lead to low bone mineral density, which will cause osteopenia, osteoporosis, and other bone disorders. To date, the mechanism of how osteoclast precursors differentiate into mature osteoclasts remains elusive. MicroRNAs (miRNAs) are novel regulatory factors that play an important role in numerous cellular processes, including cell differentiation and apoptosis, by post-transcriptional regulation of genes. Recently, a number of studies have revealed that miRNAs participate in bone homeostasis, including osteoclastic bone resorption, which sheds light on the mechanisms underlying osteoclast differentiation. In this review, we highlight the miRNAs involved in regulating osteoclast differentiation and bone resorption, and their roles in osteoporosis.

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“…These data indicate that miR-155 is involved in the commitment switch of hematopoietic precursors (Mann et al 2010). Zhang et al (2012b) revealed that miR-155 is inhibited by IFNb during osteoclast differentiation, and they identified the effect of miR-155 on the 3 0 -UTR of MITF and suppressor of cytokine signaling 1 (SOCS1). Moreover, miR-155 has been observed to be involved in the pathogenesis of autoimmune arthritis in mice, being proposed as a novel target for the treatment of RA (Bluml et al 2011).…”

Section: Mirnas and Osteoclast Differentiationmentioning

confidence: 85%

MicroRNAs and post-transcriptional regulation of skeletal development

Gámez¹,

Rodríguez-Carballo²,

Ventura³

2014

Journal of Molecular Endocrinology

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MicroRNAs (miRNAs) have become integral nodes of post-transcriptional control of genes that confer cellular identity and regulate differentiation. Cell-specific signaling and transcriptional regulation in skeletal biology are extremely dynamic processes that are highly reliant on dose-dependent responses. As such, skeletal cell-determining genes are ideal targets for quantitative regulation by miRNAs. So far, large amounts of evidence have revealed a characteristic temporal miRNA signature in skeletal cell differentiation and confirmed the essential roles that numerous miRNAs play in bone development and homeostasis. In addition, microarray expression data have provided evidence for their role in several skeletal pathologies. Mouse models in which their expression is altered have provided evidence of causal links between miRNAs and bone abnormalities. Thus, a detailed understanding of the function of miRNAs and their tight relationship with bone diseases would constitute a powerful tool for early diagnosis and future therapeutic approaches.

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Interferon‐β‐induced miR‐155 inhibits osteoclast differentiation by targeting SOCS1 and MITF

Cited by 111 publications

References 43 publications

Identification and Characterization of MicroRNA Differentially Expressed in Macrophages Exposed to Porphyromonas gingivalis Infection

Identification and Characterization of MicroRNA Differentially Expressed in Macrophages Exposed to Porphyromonas gingivalis Infection

The role of MicroRNAs in Osteoclasts and Osteoporosis

MicroRNAs and post-transcriptional regulation of skeletal development

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