LncRNA NEAT1/miR-29b-3p/BMP1 axis promotes osteogenic differentiation in human bone marrow-derived mesenchymal stem cells

Zhang, Yingzi; Chen, Bin; Li, Dazhuang; Zhou, Xiaozhong; Chen, Zhiwei

doi:10.1016/j.prp.2018.12.034

Cited by 74 publications

(57 citation statements)

References 30 publications

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“…( 10 ) Neat1 enhances the assembly and activation of the inflammasomes nucleotide‐binding domain like receptor protein 3 (NLRP3), NLR family caspase activation and recruitment domain–containing protein 4 (NLRC4), cytosolic DNA sensors, absent in melanoma 2 (AIM2) in macrophages. ( 11 ) A recent study revealed that NEAT1 is significantly higher in osteoporosis patients compared with normal controls, and regulates BMP1 through competitively binding with microRNA miR‐29b‐3p, ( 12 ) indicating its potential role in bone metabolism and osteoporosis. However, the concrete mechanisms of Neat1 in bone metabolism, especially in osteoclast formation and function, are still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

lncRNA Neat1 Stimulates Osteoclastogenesis Via Sponging miR-7

Zhang

Chen

et al. 2020

Journal of Bone and Mineral Research

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Increasing evidence uncover the essential role of long noncoding RNA (lncRNAs) in bone metabolism and the association of lncRNA with genetic risk of osteoporosis. However, whether lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) is involved remains largely unknown. In the present study, we found that Neat1 is induced by osteoclastic differentiation stimuli. Knockdown of Neat1 attenuates osteoclast formation whereas overexpression of Neat1 accelerates osteoclast formation. In vivo evidence showed that enhanced Neat1 expression stimulates osteoclastogenesis and reduces bone mass in mice. Mechanically, Neat1 competitively binds with microRNA 7 (miR‐7) and blocks its function for regulating protein tyrosine kinase 2 (PTK2). Intergenic SNP rs12789028 acts as allele‐specific long‐range enhancer for NEAT1 via chromatin interactions. We establish for the first time that Neat1 plays an essential role in osteoclast differentiation, and provide genetic mechanism underlying the association of NEAT1 locus with osteoporosis risk. These results enrich the current knowledge of NEAT1 function, and uncover the potential of NEAT1 as a therapeutic target for osteoporosis. © 2020 American Society for Bone and Mineral Research.

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Section: Introductionmentioning

confidence: 99%

lncRNA Neat1 Stimulates Osteoclastogenesis Via Sponging miR-7

Zhang

Chen

et al. 2020

Journal of Bone and Mineral Research

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“…The lncRNA NEAT1 and MALAT1 are often considered to be tumor-related lncRNAs, 44 but evidence also correlates these lncRNA with osteogenic differentiation. [45][46][47][48] Several studies show that NEAT1 and MALAT1 promote osteoblast differentiation by sponging miRNAs such as miR-214 and miR-204. [46][47][48] In contrast, Li et al 45 showed that silencing MALAT1 in lipopolysaccharide-treated chondrocytes promoted IL-6 expression and apoptosis by sponging and inactivating miR-146a.…”

Section: Discussionmentioning

confidence: 99%

Identification of the specific microRNAs and competitive endogenous RNA mechanisms in osteoporosis

Hong

et al. 2020

J Int Med Res

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Objective Osteoporosis and osteoarthritis are metabolic skeletal disorders. This study aimed to identify specific networks of competitive endogenous RNA (ceRNA) in osteoporosis that differ from those in osteoarthritis. Methods The dataset GSE74209 was downloaded from the Gene Expression Omnibus, and differentially expressed microRNAs (DEmiRNAs) in osteoporotic samples and osteoarthritic samples were identified. After predicting target genes and linked long noncoding (lnc)RNAs, ceRNA networks of DEmiRNAs were constructed. The nodes that overlapped between ceRNA networks and the Comparative Toxicogenomics Database were selected as key candidates. Results Fifteen DEmiRNAs (including 2 downregulated and 13 upregulated miRNAs) were identified in osteoporotic samples versus osteoarthritic samples; these targeted 161 genes and linked to 60 lncRNAs. The ceRNA network consisted of 6 DEmiRNAs, 63 target genes, and 53 lncRNAs. After searching the Comparative Toxicogenomics Database and mining the literature, 2 lncRNAs ( MALAT1 and NEAT1), 2 DEmiRNAs ( hsa- miR- 32-3p, downregulated; and hsa-miR-22-3p, upregulated) and 6 genes ( SP1, PTEN, ESR1, ERBB3, CSF1R, and CDK6) that relate to cell death, growth, and differentiation were identified as key candidates separating osteoporosis from osteoarthritis. Conclusions Two miRNA–ceRNA networks (including NEAT1/ MALAT1- hsa- miR- 32- 3p- SP1/ FZD6 and NEAT1/ MALAT1- hsa- miR- 22- 3p- PTEN/ ESR1/ ERBB3/ CSF1R/ CDK6) might have crucial and specific roles in osteoporosis.

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“…For example, Wang et al reported that lncRNA KCNQ1OT1 promoted osteogenic differentiation through absorbing miR-374a to upregulate BMP2 [20]. Zhang et al identi ed NEAT1 promoted BMP1 expression to regulate osteogenic differentiation of hBMSCs by sponging miR-29b-3p [21]. In addition, miRNAs have been reported to be involved in the occurrence of bone metabolic diseases [22].…”

Section: Discussionmentioning

confidence: 99%

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

Gao

Xue

Yang

2020

Preprint

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Objective: This study aims to illustrate the underlying molecular mechanisms of long noncoding RNAs (LncRNAs) LINC00899 in osteoporosis.Methods: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) used to examine the levels of LINC00899, miR-374a and RUNX2 in clinical tissues or human bone mesenchymal stem cells (hBMSCs). The interaction between miR-374a and LINC00899 or RUNX2 was predicted by starBase and verified by luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. Results: The expression of LINC00899 was lowly expressed in osteoporotic patients’ bone tissues and knockdown of LINC00899 decreased the expression of osteogenesis-related genes. Moreover, LINC00899 was confirmed to inhibit miR-374a expression by direct interaction. the expression levels of LINC00899 were gradually increased, but miR-374a expression was decreased with the prolongation of osteogenic induction. Finally, we demonstrated that RUNX2 was a target of miR-374a, and the silencing of miR-374a partially abolished the inhibitory effect of LINC00899 knockdown on the expression of RUNX2, OPN and OCN.Conclusions: We demonstrated that LINC00899 facilitated osteogenic differentiation of hBMSCs and prevent osteoporosis by sponging miR-374a and enhancing RUNX2 expression, which might provide a useful therapeutic strategy for osteoporosis patients.

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LncRNA NEAT1/miR-29b-3p/BMP1 axis promotes osteogenic differentiation in human bone marrow-derived mesenchymal stem cells

Cited by 74 publications

References 30 publications

lncRNA Neat1 Stimulates Osteoclastogenesis Via Sponging miR-7

lncRNA Neat1 Stimulates Osteoclastogenesis Via Sponging miR-7

Identification of the specific microRNAs and competitive endogenous RNA mechanisms in osteoporosis

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

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