miR-182 is a negative regulator of osteoblast proliferation, differentiation, and skeletogenesis through targeting FoxO1

Kim, Kyoung Min; Park, Su Jin; Jung, Seung Hyun; Kim, Eun Jin; Gadi, Jogeswar; Ajita, Jami; Rhee, Yumie; Kim, Cheol-Hee; Lim, Sung Kil

doi:10.1002/jbmr.1604

Cited by 154 publications

(132 citation statements)

References 40 publications

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“…**p < 0.01. such as MIR182, may be responsible for regulating the FOXO1 protein level when an increase in FOXO1 mRNA is observed. 57,58 MicroRNAs bind to the 3'UTR of the mRNA of specific genes and suppress their translation, 59 thus preventing changes in protein expression despite changes in the mRNA level. Future studies should investigate whether microRNAs are involved in the regulation of FOXO1 translation.…”

Section: Discussionmentioning

confidence: 99%

FOXO3 induces FOXO1-dependent autophagy by activating the AKT1 signaling pathway

et al. 2012

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Abbreviations: ATG, autophagy related; FOXO1, forkhead box O1; FOXO3, forkhead box O3; GFP, green fluorescent protein; MAP1LC3, microtubule-associated protein 1 light chain 3; PIK3CA, class I PI3K catalytic subunit the BECN1-PtdIns3K complex to promote autophagosome formation. 16,17 Recent evidence has revealed that the FOXO protein family members FOXO1 and FOXO3 promote autophagy. [18][19][20][21][22][23] In skeletal muscle cells, FOXO3 directly upregulates autophagy-related genes, such as microtubule-associated protein 1 light chain 3 (MAP1LC3) and BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3).19 FOXO1 has both transcription-dependent and transcription-independent roles in autophagy. In mouse cardiomyocytes, FOXO1 is deacetylated by the NAD-dependent deacetylase sirtuin-1 (SIRT1) that, in turn, induces the expression of the RAS-related GTP-binding protein RAB7A, which mediates the fusion of mature autophagic vesicles with lysosomes. 21 In addition, FOXO1 mediates starvation-induced autophagy through a transcription-independent mechanism in human cancer cells. We have previously observed that cytoplasmic FOXO1 is required for serum starvation-or H 2 O 2 -induced autophagy in cancer cells. Under these conditions, FOXO1 became acetylated and dissociated from SIRT2 in the cytoplasm, and the acetylated FOXO1, in turn, binds to ATG7 to promote autophagy. 23 Therefore, it is ©2012 Landes Bioscience. Do not distribute.www.landesbioscience.com Autophagy

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Section: Discussionmentioning

confidence: 99%

FOXO3 induces FOXO1-dependent autophagy by activating the AKT1 signaling pathway

et al. 2012

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“…51 In particular, several recent studies revealed that FoxO1 is able to promote osteoblast differentiation of the progenitor cells. 20,21,[52][53][54] However, its role in regulating osteogenic differentiation of ADSCs has not been reported yet. The data obtained from the present Western blot analysis showed that in human ADSCs, expression of FoxO1 was upregulated after addition of the osteogenic medium, and more importantly, cotreatment of fullerol with the osteogenic medium further augmented expression of this transcript factor and its significant targets Runx2, OCN, and SOD2 ( Figure 5).…”

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confidence: 99%

Antioxidative fullerol promotes osteogenesis of human adipose-derived stem cells

Yang¹,

Li²,

Wan³

et al. 2014

IJN

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Antioxidants were implicated as potential reagents to enhance osteogenesis, and nano-fullerenes have been demonstrated to have a great antioxidative capacity by both in vitro and in vivo experiments. In this study, we assessed the impact of a polyhydroxylated fullerene, fullerol, on the osteogenic differentiation of human adipose-derived stem cells (ADSCs). Fullerol was not toxic against human ADSCs at concentrations up to 10 μM. At a concentration of 1 μM, fullerol reduced cellular reactive oxygen species after a 5-day incubation either in the presence or in the absence of osteogenic media. Pretreatment of fullerol for 7 days increased the osteogenic potential of human ADSCs. Furthermore, when incubated together with osteogenic medium, fullerol promoted osteogenic differentiation in a dose-dependent manner. Finally, fullerol proved to promote expression of FoxO1, a major functional isoform of forkhead box O transcription factors that defend against reactive oxygen species in bone. Although further clarification of related mechanisms is required, the findings may help further development of a novel approach for bone repair, using combined treatment of nano-fullerol with ADSCs.

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“…In addition, microRNAs (miRNAs) regulate gene expression at the post-transcriptional level and were recently shown to move between cells via gap junctions [28,29]; therefore, these small regulatory RNAs may be transported across gap junctions from MLO-A5 cells to 10T-GFP cells. The actions of miRNAs are the subject of increasing attention in a variety of fields [30][31][32]; in a recent study, overexpression of miR218 increased the expression 224 MIKAMI ET AL.…”

Section: Discussionmentioning

confidence: 99%

Osteogenic Gene Transcription Is Regulated via Gap Junction-Mediated Cell–Cell Communication

Mikami

Yamamoto²,

Akiyama³

et al. 2015

Stem Cells and Development

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An analytical study of cell-cell communications between murine osteoblast-like MLO-A5 cells and bone marrow mesenchymal stem cell (BMSC)-like C3H10T1/2 cells was performed. C3H10T1/2 cells expressing green fluorescent protein (10T-GFP cells) were generated to enable the isolation of the BMSC-like cells from co-cultures with MLO-A5 cells. The mRNA expression levels of several osteogenic transcription factors (Runx2, Osterix, Dlx5, and Msx2) did not differ between the co-cultured and mono-cultured 10T-GFP cells, but those of alkaline phosphatase (ALP) and bone sialoprotein (BSP) were 300-to 400-fold higher in the cocultured cells. Patch clamp and biocytin transfer assays revealed gap junction-mediated communication between co-cultured 10T-GFP and MLO-A5 cells. The addition of a gap junction inhibitor suppressed the increases in the expression levels of the ALP and BSP mRNAs in co-cultured 10T-GFP cells. Furthermore, the histone acetylation levels were higher in co-cultured 10T-GFP cells than in mono-cultured 10T-GFP cells. These results suggest that osteoblasts and BMSCs associate via gap junctions, and that gap junction-mediated signaling induces histone acetylation that leads to elevated transcription of the genes encoding ALP and BSP in BMSCs.

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miR-182 is a negative regulator of osteoblast proliferation, differentiation, and skeletogenesis through targeting FoxO1

Cited by 154 publications

References 40 publications

FOXO3 induces FOXO1-dependent autophagy by activating the AKT1 signaling pathway

FOXO3 induces FOXO1-dependent autophagy by activating the AKT1 signaling pathway

Antioxidative fullerol promotes osteogenesis of human adipose-derived stem cells

Osteogenic Gene Transcription Is Regulated via Gap Junction-Mediated Cell–Cell Communication

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