Long non-coding RNA MALAT1 promotes odontogenic differentiation of human dental pulp stem cells by impairing microRNA-140-5p-dependent downregulation of GIT2

Bao, Mu-rong; Liu, Gaoxia; Song, Jia L.; Gao, Yidan

doi:10.1007/s00441-020-03246-1

Cited by 18 publications

(15 citation statements)

References 31 publications

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“…The molecular mechanisms of tooth regeneration were complex and it was regulated by gene network through the interaction of numerous signaling pathways and growth factors [28,29]. An increasing amount of lncRNAs, such as H19 [19] and MALAT1 [30], had been discovered to have important regulatory effects in the osteo/odontogenic differentiation of dental stem cells. To date, only a few lncRNAs related to osteo/odontogenesis of SCAPs have been well discovered in the published literature.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: LncRNA NHS-AS1 regulates osteo/odontogenic differentiation of stem cells from apical papilla via miR-5011-5p/SMAD7 axis

Yang

et al. 2022

Preprint

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Background: Elucidating the osteo/odontogenic differentiation mechanisms in human stem cells from apical papilla (SCAPs) is the key to promoting dentin regeneration. A growing number of studies have identified long non-coding RNAs (lncRNAs) as key roles in osteogenesis. Nonetheless, their functions and mechanisms in osteo/odontogenic differentiation of SCAPs have yet to be clarified. Methods: We analyzed the expression profiles of lncRNAs between the osteo/odontogenic differentiation group and control group by lncRNAs microarray and found NHS-AS1 was a key factor during the osteo/odontogenic differentiation of SCAPs, as evidenced by quantitative real-time PCR (qRT-PCR). Explored the function of NHS-AS1 by transfecting NHS-AS1 overexpression plasmid vectors into SCAP cells. qRT-PCR, Western blot, alkaline phosphatase (ALP) staining and alizarin red staining (ARS) were used to detect changes in osteo/odontogenesis-related indicators. Bioinformatics analysis indicated that NHS-AS1 could sponge miR-5011-5p and miR-5011-5p could target SMAD7, which were further affirmed by dual luciferase reporter assay. The role of miR-5011-5p and SMAD7 in the osteo/odontogenic differentiation of SCAP were also clarified by cell transfection techniques. We performed co-transfection experiments to confirm the involvement of miR-5011-5p and SMAD7 in NHS-AS1-mediated osteo/odontogenic differentiation of SCAP.Results: The expression of NHS-AS1 was down-regulated after osteo/odontogenesis of SCAP. Over-expression of NHS-AS1 significantly inhibited the osteo/odontogenesis of SCAPs. Dual luciferase reporter assay demonstrated NHS-AS1 could sponge miR-5011-5p. Further study showed that miR-5011-5p mimics promoted osteo/odontogenic differentiation of SCAPs and reversed NHS-AS1’s inhibitory impact on the process. Meanwhile, as the target gene of miR-5011-5p, SAMD7 depressed the osteo/odontogenic differentiation of SCAPs and could overcome the positive influence of miR-5011-5p mimics on the process. NHS-AS1 competitively sponged miR-5011-5p and alleviated the suppressive action of miR-5011-5p against SMAD7 expression, thereby significantly inhibiting the osteo/odontogenic differentiation of SCAPs. Conclusion: NHS-AS1 inhibits the osteo/odontogenic differentiation of SCAPs via miR-5011-5p/SMAD7 axis.

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Section: Discussionmentioning

confidence: 99%

WITHDRAWN: LncRNA NHS-AS1 regulates osteo/odontogenic differentiation of stem cells from apical papilla via miR-5011-5p/SMAD7 axis

Yang

et al. 2022

Preprint

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“…Human DPSCs were seeded in 24‐well plates at a density of 1 × 10 4 cells/ml and incubated in osteogenic media (OM, supplemented with 100 nM dexamethasone (Sigma–Aldrich), 10 mM β‐glycerophosphate (Sigma–Aldrich), and 50 µg/ml ascorbic acid (Sigma–Aldrich) for 7 days (Bao et al, 2020). Then, human DPSCs were fixed with 4% paraformaldehyde (PFA) for 30 min and washed twice with PBS.…”

Section: Methodsmentioning

confidence: 99%

Effects of BMAL1 on dentinogenic differentiation of dental pulp stem cells via PI3K/Akt/mTOR pathway

Zhao

Chen

et al. 2022

Int Endodontic J

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Aim: This study aimed to investigate the effect of the circadian clock gene Bmal1 on dentinogenic differentiation of dental pulp stem cells (DPSCs) under inflammatory conditions.Methodology: Dental pulp stem cells were isolated from the pulp tissue of the healthy donor and were then stimulated with different concentrations of lipopolysaccharide (LPS) to mimic inflammatory conditions. Real-time polymerase chain reaction was used to detect the gene expression of circadian clock genes Bmal1, Clock, Per1, Per2, Cry1, and Cry2. Western blot (WB) was applied to analyse the protein expression of circadian clock proteins (BMAL1, CLOCK) and dentinogenic differentiation-related proteins (DSPP, DMP1). In addition, the apoptosis and osteogenic differentiation of DPSCs were also analysed in the presence of different concentrations of LPS. Results:The expression of circadian clock genes of DPSCs significantly changed in an inflammatory environment. WB analysis shows that BMAL1 is relevant to the dentinogenic differentiation of DPSCs. In low concentrations of LPS-mimicked inflammatory conditions, the expression of BMAL1 increased and promoted the dentinogenic differentiation of DPSCs. However, under high concentrations of LPSmimicked inflammatory conditions, the expression of BMAL1 decreased and inhibited the dentinogenic differentiation of DPSCs. Moreover, the effects of BMAL1 on dentinogenic differentiation of DPSCs may be through PI3K/Akt/mTOR pathway. Conclusions:This study showed that the circadian clock gene Bmal1 affected dentinogenic differentiation of DPSCs, providing a new insight for clinical stem cell-based restorative dentinogenesis therapies.

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“…MiR-3064-5p inhibits the FOXA1/CD24/Src pathway to exert an antiangiogenic effect, whereas MALAT1 adsorbs miR-3064-5p, thereby alleviating the inhibition of FOXA1 and promoting hepatic hemangiogenesis ( 44 ). Hou et al ( 45 , 46 ) confirmed that MALAT1 is an important upstream target of miR-140, which inhibits VEGF-A expression and M2 macrophage polarization, thereby inhibiting angiogenesis and immunosuppression.…”

Section: Malat1—a Regulating Role In Liver Regenerationmentioning

confidence: 97%

Long Non-coding RNA MALAT1: A Key Player in Liver Diseases

Lü

Guo

et al. 2022

Front. Med.

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Long non-coding RNAs (lncRNAs) exceed 200 nucleotides in length are considered to be involved in both developmental processes and various diseases. Here, we focus on lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), which was one of the most important lncRNAs in proliferation, apoptosis, and migration. MALAT1 plays a regulatory role in liver diseases, including hepatic fibrosis, liver regeneration, liver cancer, and fatty liver diseases. In the current review, we summarize the latest literature about the function roles of MALAT1 in liver disorders. Probing the regulatory mechanism and cross talk of MALAT1 with other signaling pathways of pathological processes would improve the prognosis, diagnosis of liver diseases, and offer a promising candidate target for therapeutic interventions.

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Long non-coding RNA MALAT1 promotes odontogenic differentiation of human dental pulp stem cells by impairing microRNA-140-5p-dependent downregulation of GIT2

Cited by 18 publications

References 31 publications

WITHDRAWN: LncRNA NHS-AS1 regulates osteo/odontogenic differentiation of stem cells from apical papilla via miR-5011-5p/SMAD7 axis

WITHDRAWN: LncRNA NHS-AS1 regulates osteo/odontogenic differentiation of stem cells from apical papilla via miR-5011-5p/SMAD7 axis

Effects of BMAL1 on dentinogenic differentiation of dental pulp stem cells via PI3K/Akt/mTOR pathway

Long Non-coding RNA MALAT1: A Key Player in Liver Diseases

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