Expression profiling of micro<scp>RNA</scp>s in <scp>RAW</scp>264.7 cells treated with a combination of tumor necrosis factor alpha and <scp>RANKL</scp> during osteoclast differentiation

Kagiya, Tadayoshi; Nakamura, Seiji

doi:10.1111/jre.12017

Cited by 109 publications

(129 citation statements)

References 51 publications

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“…48 Kopriva et al 49 observed that toll-like receptor 3 activation induces placental miR-210 through hypoxia-inducible factor-1α and the nuclear factor-κB-p50 pathway, leading to a decrease in signal transducer and activator of transcription 6, interleukin-4 induced, and interelukin-4 levels, which may contribute to the development of preeclampsia. In this study, we found that TNF-α significantly increased the expression of miR-210 in HTR-8/ SVneo cells, which is similar to the observation of Kagiya et al 29 in murine macrophage cell line, RAW264.7 cells. Meanwhile, the KCMF1 expression was downregulated on TNF-α treatment.…”

Section: Discussionsupporting

confidence: 78%

“…Tumor necrosis factor-α (TNF-α) has been reported as one of the regulators of miR-210 in other cell type, 29 and this inflammatory factor increased significantly in the fetal-maternal interface of patients with preeclampsia. [30][31][32][33][34] We treated HTR8/SVneo cells with recombinant human TNF-α and examined miR-210 and KCMF1 levels after 24 hours.…”

Section: Tnf-α Increases Mir-210 Expression But Downregulates Kcmf1mentioning

confidence: 99%

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MicroRNA-210 Contributes to Preeclampsia by Downregulating Potassium Channel Modulatory Factor 1

Luo

Shao

et al. 2014

Hypertension

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C omplicating 7% to 10% of pregnancies, 1 preeclampsia, along with other hypertensive disorders of pregnancy, is a major contributor to maternal morbidity worldwide. 2,3Although abnormal placentation is thought to play a major role in the development of preeclampsia, the pathogenesis of this disorder is not clearly understood. 4 Defects of trophoblast cell function, such as reduced proliferation, 5 excessive apoptosis, 6 aberrant differentiation, 7 limited migration and invasion of the uterus, and poor remodeling of spiral arteries, 8,9 have been considered to be associated with preeclampsia. Nevertheless, the molecular mechanisms underlying the onset and progression of preeclampsia remain largely unknown.MicroRNAs are 22-to 24-nucleotide noncoding RNAs that regulate gene expression by seed sequence pairing with the 3′-untranslated region (UTR) of target mRNAs, leading to repressed translation or induced mRNA cleavage of the target genes. 10,11 MicroRNAs have been identified as essential mediators of numerous cellular processes, 12 potentially including the response to hypoxia. In particular, microRNA-210 (miR-210) is specifically induced by hypoxia-inducible factor-1α during hypoxia 13 and regulates many hypoxia response pathways, including cell survival, 14 angiogenesis, mitochondrial metabolism, 15 and DNA repair. 16 miR-210 can target and suppress a large number of genes, including the cell cycle regulator E2F transcription factor 3, 17 the receptor tyrosine kinase ligand ephrinA3, 18 the DNA repair protein RAD52, 19 and the iron-sulfur cluster assembly proteins 1/2. 15 Recent studies revealed that miR-210 was upregulated in patients with preeclampsia [20][21][22][23][24] and demonstrated that hypoxia-inducible miR-210 might participate in the occurrence of preeclampsia via the downregulation of ephrin-A3 and homeobox-A9. 24 The repressive effect of miR-210 on primary trophoblast cell invasion was also reported. 23 In addition, the study by us and others revealed that miR-210 could be a potential serum biomarker Abstract-Preeclampsia is a pregnancy-specific syndrome manifested by the onset of hypertension and proteinuria after the 20th week of gestation. Abnormal placenta development has been generally accepted as the initial cause of the disorder. Recently, microRNA-210 (miR-210) has been found to be upregulated in preeclamptic placentas compared with normal placentas, indicating a possible association of this small molecule with the placental pathology of preeclampsia. However, the function of miR-210 in the development of the placenta remains elusive. The aim of this study was to characterize the molecular mechanism of preeclampsia development by examining the role of miR-210. In this study, miR-210 and potassium channel modulatory factor 1 (KCMF1) expressions were compared in placentas from healthy pregnant individuals and patients with preeclampsia, and the role of miR-210 in trophoblast cell invasion via the downregulation of KCMF1 was investigated in the immortal trophoblast cell line HTR8/SVneo. Th...

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Section: Discussionsupporting

confidence: 78%

Section: Tnf-α Increases Mir-210 Expression But Downregulates Kcmf1mentioning

confidence: 99%

MicroRNA-210 Contributes to Preeclampsia by Downregulating Potassium Channel Modulatory Factor 1

Luo

Shao

et al. 2014

Hypertension

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“…miRNA participates in osteogenic differentiation from MSCs (Guo et al, 2011). Up-regulated miR-689 expression is involved in tumor necrosis factor-alpha (TNF-α)/RANKL-regulated osteoclast differentiation (Kagiya and Nakamura, 2013). miR-654-5p may play an important role in osteogenic differentiation from human bone marrow MSCsby directly suppressing themRNA and protein expressions of bone morphogenetic protein 2 (BMP2) by binding to a specific target site (Wei et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Identification of long non-coding RNA involved in osteogenic differentiation from mesenchymal stem cells using RNA-Seq data

Song¹,

Gu²,

Qian³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to identify long non-coding RNA (lncRNA) associated with osteogenic differentiation from mesenchymal stem cells (MSCs) using high-throughput RNA sequencing (RNA-Seq) data. RNA-Seq dataset was obtained from the European Bioinformatics Institute (accession No. PRJEB4496), including two replicates each for immortalized mesenchymal stem cells iMSC#3 cultured in growth medium (GM) and differentiation medium (DM) for 28 days. The clean reads were aligned to a hg19 reference genome by Tophat and assembled by Cufflinks to identify the known and novel transcripts. RPKM values were calculated to screen for differentially expressed RNA. Novel lncRNA were screened based on various filter criteria. Subsequently, the underlying function of novel lncRNAs were predicted by functional annotation by ERPIN, a coexpression network was constructed by WGCNA and the KEGG pathway enriched by KOBAS. A total of 3171 RNA differentially expressed between the DM and GM groups (2597 mRNA and 574 lncRNA) were identified. Among the 574 differentially expressed lncRNA, 357 were known and 217 were novel lncRNA. Furthermore, 32 novel lncRNA were found to be miRNA precursors (including miR-689, miR-640, miR-601, and miR-544). A total of 18269 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 18268-18279 (2015) Identifying lncRNA affecting osteogenic differentiation 14,275 co-expression relationships and 217 co-expression networks were obtained between novel lncRNA and mRNA. The differentially expressed lncRNA and mRNA were enriched into 6 significant pathways, including those for cancer, ECM-receptor interaction, and focal adhesion. Therefore, novel lncRNAwere identified and their underlying function predicted, which may provide the basis for future analyses of the role of lncRNA in osteoblastic differentiation.

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“…RAW264.7 cells were tested by FISH analysis and found to be diploid at least on chromosomes 7,8,11,16, and 17, and were kindly provided by Prof. P. Tsichlis (Tufts Medical School, Boston, MA). E. coli-derived LPS (100 ng/ml; O111:B4; catalog no.…”

Section: Cell Culturementioning

confidence: 99%

“…In humans, miR-146a appears to be important in the development of innate immune tolerance observed in leukemic patients (8). Both miRs have attracted particular attention, because they are responsive to a plethora of inflammatory stimuli including TLR ligands, TNFa, IL-1b, type I and type II IFNs, or RANKL in different cell types, including macrophages (9)(10)(11)(12)(13)(14)(15)(16). miR-155 and miR-146a target and repress several downstream TLR4 mediators such as TNF-a, PU.1, SHIP1, SOCS1 and TNFR-associated factor-6, IRAK1, and IRF5, respectively, highlighting their pivotal role in the development of endotoxin tolerance (1).…”

mentioning

confidence: 99%

Coordinated Regulation of miR-155 and miR-146a Genes during Induction of Endotoxin Tolerance in Macrophages

Doxaki

Kampranis

Eliopoulos

et al. 2015

The Journal of Immunology

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Endotoxin tolerance occurs to protect the organism from hyperactivation of innate immune responses, primarily mediated by macrophages. Regulation of endotoxin tolerance occurs at multiple levels of cell responses and requires significant changes in gene expression. In the process of macrophage activation, induced expression of microRNA (miR)-155 and miR-146a contributes to the regulation of the inflammatory response and endotoxin tolerance. In this article, we demonstrate that expression of both miRNAs is coordinately regulated during endotoxin tolerance by a complex mechanism that involves monoallelic interchromosomal association, alterations in histone methyl marks, and transcription factor binding. Upon activation of naive macrophages, Histone3 was trimethylated at lysine4 and NFκBp65 was bound on both miR-155 and miR-146a gene loci. However, at the stage of endotoxin tolerance, both miR gene loci were occupied by C/EBPβ, NFκBp50, and the repressive Histone3 marks trimethylation of K9 of H3. DNA fluorescence in situ hybridization experiments revealed monoallelic interchromosomal colocalization of miR-155 and miR-146a gene loci at the stage of endotoxin tolerance, whereas RNA-DNA-fluorescence in situ hybridization experiments showed that the colocalized alleles were silenced, suggesting a common repression mechanism. Genetic ablation of Akt1, which is known to abrogate endotoxin tolerance, abolished induction of loci colocalization and C/EBPβ binding, further supporting that this mechanism occurs specifically in endotoxin tolerance. Overall, this study demonstrates that two miRNAs are coordinately regulated via gene colocalization at the three-dimensional chromatin space, same transcriptional machinery, and similar Histone3 methylation profile, contributing to the development of endotoxin tolerance.

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Expression profiling of microRNAs in RAW264.7 cells treated with a combination of tumor necrosis factor alpha and RANKL during osteoclast differentiation

Abstract: These results suggest that miR-223 and miR-378 may play important roles in osteoclastogenesis, and that miR-21, miR-29b, miR-146a, miR-155 and miR-210 are involved in TNF-α-regulated osteoclast differentiation.

Cited by 109 publications

References 51 publications

MicroRNA-210 Contributes to Preeclampsia by Downregulating Potassium Channel Modulatory Factor 1

MicroRNA-210 Contributes to Preeclampsia by Downregulating Potassium Channel Modulatory Factor 1

Identification of long non-coding RNA involved in osteogenic differentiation from mesenchymal stem cells using RNA-Seq data

Coordinated Regulation of miR-155 and miR-146a Genes during Induction of Endotoxin Tolerance in Macrophages

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