MicroRNA‐195‐5p Regulates Osteogenic Differentiation of Periodontal Ligament Cells Under Mechanical Loading

Chang, Maolin; Lin, Heng; Fu, Haidi; Wang, Beike; Hân, Gia; Fan, Mingwen

doi:10.1002/jcp.25856

Cited by 64 publications

(60 citation statements)

References 46 publications

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“…In the tension side of the OTM, new bone forms as a result of tensile strain on the PDLCs. Accordingly, the expressions of osteogenic markers in PDLCs, such as core‐binding factor α1 (Cbfα1, also known as RUNX2), osterix (OSX), osteocalcin (OCN), collagen type I (COL I), and alkaline phosphatase (ALP), are found to be elevated under tensile strain, suggesting an osteoblastic phenotype of PDLCs …”

Section: Introductionmentioning

confidence: 99%

“…Accordingly, the expressions of osteogenic markers in PDLCs, such as core-binding factor α1 (Cbfα1, also known as RUNX2), osterix (OSX), osteocalcin (OCN), collagen type I (COL I), and alkaline phosphatase (ALP), are found to be elevated under tensile strain, suggesting an osteoblastic phenotype of PDLCs. [4][5][6][7] Transcriptional co-activator with PDZ-binding motif (TAZ) is a key component of hippo pathway that participates in a wide range of cellular activities including proliferation, tumorigenesis, and stem cell self-renewal, through the interaction with transcription factors in a context-dependent manner. 8 Recently, increasing attention has also been paid to the role of TAZ in osteogenesis of stem cells, which is associated with the co-activation and binding of Cbfα1, a transcription factor that is required for osteoblastic differentiation.…”

Section: Introductionmentioning

confidence: 99%

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TAZ contributes to osteogenic differentiation of periodontal ligament cells under tensile stress

Wang

et al. 2019

J of Periodontal Research

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Background and objective Bone remodeling during orthodontic treatment is achieved by the osteogenesis of human periodontal ligament cells (PDLCs) subjected to mechanical loadings. Transcriptional co‐activator with PDZ‐binding motif (TAZ) mediates bone remodeling in response to extracellular mechanical signals. This study aims to investigate the role of TAZ in osteogenesis of PDLCs under tensile strain. Materials and methods A uniaxial cyclic tensile stress (CTS) at 12% elongation and 6 cycles/min (5 s on and 5 s off) was applied to PDLCs. The osteogenic differentiation was determined by the protein and gene expressions of osteogenic markers using qRT‐PCR and Western blot, respectively, and further by alkaline phosphatase (ALP) activity and Alizarin Red S staining. The interaction of TAZ with core‐binding factor α1 (Cbfα1) was examined by co‐immunoprecipitation. The immunofluorescence histochemistry was used to examine the nucleus aggregation of TAZ and the reorganization of actin filaments. Moreover, small interfering RNA‐targeting TAZ (TAZsiRNA) was used for TAZ inhibition and Y‐27632 was employed for Ras homologue‐associated coiled‐coil protein kinase (ROCK) signaling blockage. Results CTS clearly stimulated the nucleus accumulation of TAZ and its interaction with Cbfα1. CTS‐induced osteogenesis in PDLCs was significantly abrogated by the infection with TAZsiRNA, as shown by the decreased stained nodules and protein expressions of Cbfα1, collagen type I, osterix, and osteocalcin, along with the inhibition of β‐catenin signaling. Moreover, ROCK inhibition by Y‐27632 hindered TAZ nucleus aggregation and its binding with Cbfα1, which subsequently lead to the decreased osteoblastic differentiation of PDLCs. Conclusions Taken together, we propose that TAZ nucleus localization and its interaction with Cbfα1 are essential for the CTS‐induced osteogenic differentiation in PDLCs. And such TAZ activation by CTS could be mediated by ROCK signaling, indicating the pivot role of ROCK‐TAZ pathway for PDLCs differentiation.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TAZ contributes to osteogenic differentiation of periodontal ligament cells under tensile stress

Wang

et al. 2019

J of Periodontal Research

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“…Pdlcs are mechanically sensitive cells that may be induced by mechanical force, and they express a series of cytokines, including macrophage colony stimulating factor (M-cSF), receptor activator of nF-κB ligand (ranKl), osteoprotegerin (OPG) and inflammatory factors (2,3). The combined functional interventions that result from these factors serve to control the development of alveolar bone (4,5).…”

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confidence: 99%

The roles of mechanosensitive ion channels and associated downstream MAPK signaling pathways in PDLC mechanotransduction

et al. 2020

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The present study aimed to investigate whether the cytoskeleton, the Piezo1 ion channel and the transient receptor potential cation channel subfamily V member 4 (TrPV4) ion channel are equally functional in the mechanotransduction of periodontal ligament cells (Pdlcs) and to reveal the interplay of these mechanically sensitive ion channels (MScs). Human Pdlcs (hPdlcs) were pretreated with cytochalasin d (the inhibitor of actin polymerization), GsMTx4 (the antagonist of Piezo1) and GSK205 (the antagonist of TrPV4), and then subjected to periodic mechanical loading. The expression levels of macrophage colony stimulating factor (M-cSF), receptor activator of nF-κB ligand (ranKl) and cyclooxygenase-2 (coX2) in hPdlcs were detected via western blotting. osteoblast mineralization induction capacity of the hPdlcs was also studied and the mitogen-activated protein kinase (MAPK) expression profile was determined via protein microarray. The expression of Piezo1 and TRPV4 in the PDLCs was significantly increased at 8 h after loading. These differences in expression were accompanied by increased expression of M-cSF, ranKl and coX2. compared with the control group, key Pdlc biomarkers were suppressed after mechanical loading following treatment with the inhibitors of Piezo1 (GsMTx4) and TrPV4 (GSK205). The phosphorylated-MAPK protein array showed differential biomarker profiles among all groups. The present study suggested that both MScs and the cytoskeleton participated as mechanical sensors, and did so independently in hPdlc mechanotransduction. Furthermore, the Piezo1 ion channel may transmit mechanical signals via the erK signaling pathway; however, the TrPV4 channel may function via alternative signaling pathways.

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“…In recent years, mechanical loading has been shown to promote osteogenesis in osteoblasts and BMSCs by regulating miRNAs [18][19][20][21], which suggests that exercise may regulate bone metabolism through miRNAs [22]. And whether exercise can induce changes in miRNA expression in bone is still unknown.…”

Section: Mir-214 Attenuates the Osteogenic Effects Of Mechanical Loadmentioning

confidence: 99%

MiR-214 Attenuates the Osteogenic Effects of Mechanical Loading on Osteoblasts

et al. 2019

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Exercise is an effective way to prevent osteoporosis, but its mechanism remains unclear. MicroRNAs (miRNAs) play an essential role in bone metabolism. Recently, mechanical loading was reported to induce changes in miRNA expression in osteoblasts. However, the role of miRNAs in bone under exercise and its underlining mechanisms of action still remain unknown. MiR-214 was reported to regulate the process of osteogenesis and is considered a biomarker of osteoporosis. In this study, we aimed to investigate whether exercise could induce changes in miRNA expression in bone and to study the effects of miR-214 on mechanical loading-induced osteogenesis in osteoblasts. The results showed that miR-214 was down-regulated in both tibia from C57BL/6 mice after exercise in vivo and in osteoblasts after mechanical strain in vitro. Mechanical strain could enhance the ALP activity, promote matrix mineralization, up-regulate the expression of osteogenic factors such as ATF4, Osterix, ALP and β-catenin, and down-regulate RANKL and RANK expression. Over-expression of miR-214 not only inhibited the expression of these osteogenic factors but also attenuated mechanical strain-enhanced osteogenesis in osteoblasts. Collectively, our results indicated that miR-214 could attenuate the osteogenic effects of mechanical loading on osteoblasts, suggesting that inhibition of miR-214 may be one of the ways in which exercise prevents osteoporosis.

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MicroRNA‐195‐5p Regulates Osteogenic Differentiation of Periodontal Ligament Cells Under Mechanical Loading

Cited by 64 publications

References 46 publications

TAZ contributes to osteogenic differentiation of periodontal ligament cells under tensile stress

TAZ contributes to osteogenic differentiation of periodontal ligament cells under tensile stress

The roles of mechanosensitive ion channels and associated downstream MAPK signaling pathways in PDLC mechanotransduction

MiR-214 Attenuates the Osteogenic Effects of Mechanical Loading on Osteoblasts

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