Micro<scp>RNA</scp>‐3064‐3p regulates the differentiation of cementoblasts through targeting <scp>DKK</scp>1

Wang, Chuan; Liao, Hai; Sun, Hairong; Zhang, Y.; Cao, Zhengguo

doi:10.1111/jre.12554

Cited by 21 publications

(21 citation statements)

References 50 publications

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Section: Discussioncontrasting

confidence: 99%

“…Therefore, these miRNAs can work in concert and efficiently during cementoblast commitment by interacting with each other. Some groups have reported the role of microRNAs in cementogenesis 50‐52 ; however, in this study, we did not detect the same mRNAs and microRNAs as those detected in previous reports. Taking into consideration that double overexpression of miR‐383 and miR‐628‐5p weakened the enhancement of CEMP1 and OPN mRNA expression (Figure 2), cementogenesis of MSCs likely regulates some factors, for example, Nfat5, DKK1, miR‐361‐3p, miR3064‐3p, or miR‐155‐3p, and the underlying mechanisms must be elucidated.…”

Section: Discussioncontrasting

confidence: 94%

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Identification of regulatory mRNA and microRNA for differentiation into cementoblasts and periodontal ligament cells

Iwata

Mizuno

Nagahara

et al. 2020

J of Periodontal Research

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Objective Periodontitis causes periodontal tissue destruction and results in physiological tooth dysfunction. Therefore, periodontal regeneration is ideal therapy for periodontitis. Mesenchymal stem cells (MSCs) are useful for periodontal regenerative therapy as they can differentiate into periodontal cells; however, the underlying regulatory mechanism is unclear. In this study, we attempted to identify regulatory genes involved in periodontal cell differentiation and clarify the differentiation mechanism for effective periodontal regenerative therapy. Background The cementum and periodontal ligament play important roles in physiological tooth function. Therefore, cementum and periodontal ligament regeneration are critical for periodontal regenerative therapy. Mesenchymal stem cell transplantation can be a common periodontal regenerative therapy because these cells have multipotency and self‐renewal ability, which induces new cementum or periodontal ligament formation. Moreover, MSCs can differentiate into cementoblasts. Cementoblast‐ or periodontal ligament cell–specific proteins have been reported; however, it is unclear how these proteins are regulated. MicroRNA (miRNA) can also act as a key regulator of MSC function. Therefore, in this study, we identified regulatory genes involved in cementoblast or periodontal cell differentiation and commitment. Methods Human MSCs (hMSCs), cementoblasts (HCEM), and periodontal ligament cells (HPL cells) were cultured, and mRNA or miRNA expression was evaluated. Additionally, cementoblast‐specific genes were overexpressed or suppressed in hMSCs and their expression levels were investigated. Results HCEM and HPL cells expressed characteristic genes, of which we focused on ets variant 1 (ETV1), miR‐628‐5p, and miR‐383 because ETV1 is a differentiation‐related transcription factor, miR‐628‐5p was the second‐highest expressed gene in HCEM and lowest expressed gene in HPL cells, and miR‐383 was the highest expressed gene in HCEM. miR‐628‐5p and miR‐383 overexpression in hMSCs regulated ETV1 mRNA expression, and miR‐383 overexpression downregulated miR‐628‐5p expression. Moreover, miR‐383 suppression decreased miR‐383 expression and enhanced ETV1 mRNA expression, but miR‐383 suppression also decreased miR‐628‐5p. Furthermore, silencing of ETV1 expression in hMSCs regulated miR‐628‐5p and miR‐383 expression. Concerning periodontal cell commitment, miR‐628‐5p, miR‐383, and ETV1 regulated the expression of HCEM‐ or HPL cell–related genes by adjusting the expression of these miRNAs. Conclusion HCEM and HPL cells show characteristic mRNA and miRNA profiles. In particular, these cells have specific miR‐383, miR‐628‐5p, and ETV1 expression patterns, and these genes interact with each other. Therefore, miR‐383, miR‐628‐5p, and ETV1 are key genes involved in cementogenesis or HPL cell differentiation.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 94%

Identification of regulatory mRNA and microRNA for differentiation into cementoblasts and periodontal ligament cells

Iwata

Mizuno

Nagahara

et al. 2020

J of Periodontal Research

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“…Cementoblasts, root lining cells, share similar features with osteoblasts, such as the expression of bone-associated markers, including Osterix, OCN, and BSP 29. Previous studies by our group manifested many molecules generated during cementogenesis like osteogenic markers and microRNAs are beneficial for regeneration 25, 30-32. Therefore, obtaining insights into tissue regeneration requires further understanding on the reconstruction of impaired cementum upon bacterial invasion.…”

Section: Discussionmentioning

confidence: 95%

CXXC5 Mediates P. gingivalis-suppressed Cementoblast Functions Partially via MAPK Signaling Network

Wang¹,

Liu²,

Jiang³

et al. 2019

Int. J. Biol. Sci.

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Porphyromonas (P.) gingivalis associates tightly with periodontal diseases and it is also a dominant pathogen of periapical periodontitis. However, the influence of P. gingivalis on cementoblasts, root surface cells pivotal in the apical areas, and the possible involvement of other molecules remain largely elusive. CXXC5 is a nuclear protein that regulates gene expression as well as cell growth, differentiation, and apoptosis. In this study, P. gingivalis repressed the mineralization capacity of cementoblasts by inducing inflammatory reactions and inhibiting cell differentiation. Intriguingly, the expression of CXXC5 decreased in P. gingivalis-treated OCCM-30 cells and apical periodontitis models but gradually increased during mineralization. Furthermore, RNA interference of CXXC5 significantly inhibited cementoblast differentiation, represented by decline of bone-associated markers Osterix, osteocalcin (OCN), and alkaline phosphatase (ALP). CXXC5 overexpression facilitated differentiation, and therefore attenuated the P. gingivalis-repressed effects on OCCM-30 cells. In addition, Erk1/2, p38, and PI3K-Akt were inactivated by silencing CXXC5 and activated upon its overexpression, whereas Wnt/β-catenin exhibited an opposite trend. The employment of specific inhibitors revealed that the CXXC5-dependent promotions of cementoblast differentiation were partially abrogated by p38 and PI3K-Akt inhibitors but were exacerbated by inhibiting Erk1/2. Overall, our experiment demonstrated a novel function of CXXC5 in the regeneration of impaired cementum caused by P. gingivalis invasion and suggested that MAPK signaling network balances the facilitation effects of CXXC5 in cementoblast differentiation.

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“…To fully understand the expression patterns and biological roles of miRNAs in cementoblast differentiation, we previously performed miRNA microarray profiles during cementoblast differentiation in vitro (Wang, Liao, et al 2018). We also observed that miR-3064-3p persistently decreased during cementoblast differentiation and regulated cementoblast differentiation through targeting Dickkopf-related protein 1 (DKK1).…”

Section: Introductionmentioning

confidence: 99%

MiR-361-3p/Nfat5 Signaling Axis Controls Cementoblast Differentiation

et al. 2019

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The development of periodontal tissue is a complex process, including cementoblast proliferation and differentiation. Emerging reports suggest that microRNAs (miRNAs) play crucial roles in gene regulatory networks governing numerous biological processes. However, how miRNAs modulate cementoblast proliferation and differentiation remains largely unknown. In a previous study, we performed miRNA microarray profiling to fully reveal the expression patterns of miRNAs involved in cementoblast differentiation. We focused on miR-361-3p, which decreased during cementoblast differentiation. Overexpression of miR-361-3p resulted in decreased cementoblast differentiation, whereas the functional inhibition of miR-361-3p yielded the opposite effect. The bioinformatics approach identified nuclear factor of activated T-cell 5 ( Nfat5) as a potential target of miR-361-3p, which was further verified by dual luciferase assay. Meanwhile, the expression pattern of Nfat5 was verified both in vitro and in vivo. Furthermore, knockdown of Nfat5 mimicked the inhibitory effect of overexpressing miR-361-3p in cementoblasts. Moreover, multiple signaling pathways, including the Erk1/2, JNK, p38, PI3K-Akt, and NF-κB pathways, were notably activated, and the Wnt/ß-catenin pathway was blocked by downregulation of Nfat5 or forced expression of miR-361-3p in cementoblast differentiation. Finally, the complementary approach demonstrated that miR-361-3p regulated cementoblast differentiation via or partially via Erk1/2 and PI3K-Akt. Overall, our study elucidated that the JNK, p38, NF-κB, and Wnt/ß-catenin pathways act as balancing players in the miR-361-3p/ Nfat5 signaling axis during cementoblast differentiation.

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MicroRNA‐3064‐3p regulates the differentiation of cementoblasts through targeting DKK1

Abstract: This study demonstrates, for the first time, that miR-3064-3p suppresses cementoblast differentiation via the regulation of DKK1.

Cited by 21 publications

References 50 publications

Identification of regulatory mRNA and microRNA for differentiation into cementoblasts and periodontal ligament cells

Identification of regulatory mRNA and microRNA for differentiation into cementoblasts and periodontal ligament cells

CXXC5 Mediates P. gingivalis-suppressed Cementoblast Functions Partially via MAPK Signaling Network

MiR-361-3p/Nfat5 Signaling Axis Controls Cementoblast Differentiation

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