MiR-29a is an enhancer of mineral deposition in bone-derived systems

Roberto, Vânia Palma; Tiago, Daniel M.; Silva, Iris; Cancela, M. Leonor

doi:10.1016/j.abb.2014.09.006

Cited by 32 publications

(31 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In recent years, the critical roles of miRNAs in osteogenic differentiation have been highlighted, indicating that miRNAs can serve as major regulators to promote or inhibit osteogenic differentiation [16,28,29,30]. In the present work, we have delineated that miR-24 is a negative regulator of osteogenic differentiation.…”

Section: Discussionmentioning

confidence: 61%

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1

Zhao

Dong

et al. 2015

IJMS

View full text Add to dashboard Cite

MicroRNAs (miRNAs) have been reported to have diverse biological roles in regulating many biological processes, including osteogenic differentiation. In the present study, we identified that miR-24 was a critical regulator during osteogenic differentiation. We found that overexpression of miR-24 significantly inhibited osteogenic differentiation, which decreased alkaline phosphatase activity, matrix mineralization and the expression of osteogenic differentiation markers. In contrast, inhibition of miR-24 exhibited an opposite effect. Furthermore, we delineated that miR-24 regulates post-transcriptionals of T-cell factor-1 (Tcf-1) via targeting the 3'-untranslated region (UTR) of Tcf-1 mRNA. MiR-24 was further found to regulate the protein expression of Tcf-1 in the murine osteoprogenitors cells and bone mesenchymal stem cells. Additionally, the positive effect of miR-24 suppression on osteoblast differentiation was apparently abrogated by Tcf-1 silencing. Taken together, our data suggest that miR-24 participates in osteogenic differentiation by targeting and regulating Tcf-1 expression in osteoblastic cells.

show abstract

Section: Discussionmentioning

confidence: 61%

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1

Zhao

Dong

et al. 2015

IJMS

View full text Add to dashboard Cite

show abstract

“…In more detail, the Wnt/β-catenin axis regulates osteoblast proliferation, maturation and mineralization32. Activation of the Wnt/β-catenin pathway by Wnt genes or other chemicals causes an accumulation of β-catenin in the cytoplasm and its eventual translocation into the nucleus to activate Wnt/β-catenin-responsive genes, such as c-Myc, CyclinD1, TCF-1 and LEF-1, to regulate various developmental processes, including osteogenic differentiation3334.…”

Section: Discussionmentioning

confidence: 99%

MiR-101 Targets the EZH2/Wnt/β-Catenin the Pathway to Promote the Osteogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells

Wang

Meng

Cui

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Mounting evidence indicates that microRNAs (miRNAs) are involved in multiple processes of osteogenic differentiation. MicroRNA-101 (miR-101), identified as a tumor suppressor, has been implicated in the pathogenesis of several types of cancer. However, the expression of miR-101 and its roles in the osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs) remain unclear. We found that the miR-101 expression level was significantly increased during the osteogenic differentiation of hBMSCs. MiR-101 depletion suppressed osteogenic differentiation, whereas the overexpression of miR-101 was sufficient to promote this process. We further demonstrated that enhancer of zeste homolog 2 (EZH2) was a target gene of miR-101. EZH2 overexpression and depletion reversed the promoting or suppressing effect of osteogenic differentiation of hBMSCs, respectively, caused by miR-101. In addition, we showed that miR-101 overexpression promoted the expression of Wnt genes, resulting in the activation of the Wnt/β-catenin signaling pathway by targeting EZH2, while the activity of β-catenin and the Wnt/β-catenin signaling pathway was inhibited by ICG-001, a β-Catenin inhibitor, which reversed the promoting effect of miR-101. Finally, miR-101 also promotes in vivo bone formation by hBMSCs. Collectively, these data suggest that miR-101 is induced by osteogenic stimuli and promotes osteogenic differentiation at least partly by targeting the EZH2/Wnt/β-Catenin signaling pathway.

show abstract

“…In the process of bone formation, miRNAs play essential roles in regulating osteoblast differentiation, mineral deposition by the osteoblasts, and the osteoblast’s response to mechano-stimuli3536373839. MiRNA intervention has been proposed as a candidate therapeutic modality to treat, or at least alleviate, skeletal disorders such as osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

MiR-153 Regulates Amelogenesis by Targeting Endocytotic and Endosomal/lysosomal Pathways–Novel Insight into the Origins of Enamel Pathologies

Yin

Lin

Guo

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Amelogenesis imperfecta (AI) is group of inherited disorders resulting in enamel pathologies. The involvement of epigenetic regulation in the pathogenesis of AI is yet to be clarified due to a lack of knowledge about amelogenesis. Our previous genome-wide microRNA and mRNA transcriptome analyses suggest a key role for miR-153 in endosome/lysosome-related pathways during amelogenesis. Here we show that miR-153 is significantly downregulated in maturation ameloblasts compared with secretory ameloblasts. Within ameloblast-like cells, upregulation of miR-153 results in the downregulation of its predicted targets including Cltc, Lamp1, Clcn4 and Slc4a4, and a number of miRNAs implicated in endocytotic pathways. Luciferase reporter assays confirmed the predicted interactions between miR-153 and the 3′-UTRs of Cltc, Lamp1 (in a prior study), Clcn4 and Slc4a4. In an enamel protein intake assay, enamel cells transfected with miR-153 show a decreased ability to endocytose enamel proteins. Finally, microinjection of miR-153 in the region of mouse first mandibular molar at postnatal day 8 (PN8) induced AI-like pathologies when the enamel development reached maturity (PN12). In conclusion, miR-153 regulates maturation-stage amelogenesis by targeting key genes involved in the endocytotic and endosomal/lysosomal pathways, and disruption of miR-153 expression is a potential candidate etiologic factor contributing to the occurrence of AI.

show abstract

MiR-29a is an enhancer of mineral deposition in bone-derived systems

Cited by 32 publications

References 67 publications

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1

MiR-101 Targets the EZH2/Wnt/β-Catenin the Pathway to Promote the Osteogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells

MiR-153 Regulates Amelogenesis by Targeting Endocytotic and Endosomal/lysosomal Pathways–Novel Insight into the Origins of Enamel Pathologies

Contact Info

Product

Resources

About