MicroRNA‑98‑5p prevents bone regeneration by targeting high mobility group AT‑Hook 2

Zheng, Feng; Wang, Furong; Xu, Zhe

doi:10.3892/etm.2019.7835

Cited by 9 publications

(7 citation statements)

References 34 publications

(46 reference statements)

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“…For osteogenic differentiation, MC3T3-E1 cells were cultured at 37˚C in osteogenic induction medium (25) containing 10% FBS, 100 nM dexamethasone, 5 mM L-glycerophosphate and 50 mg/ml ascorbic acid (Sigma-Aldrich; Merck KGaA) for 14 days.…”

Section: Methodsmentioning

confidence: 99%

Abnormal expression of miR‑135b‑5p in bone tissue of patients with osteoporosis and its role and mechanism in osteoporosis progression

et al. 2019

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Osteoporosis (OP) is an age-related bone disease occurring worldwide. Osteoporotic fracture is one of the leading causes of disability and death in elderly patients. MicroRNAs (miRNAs/miRs) are key molecular regulatory factors in bone remodeling processes. The present study investigated the expression and mechanism of miR-135b-5p in patients with osteoporosis. The present results suggested that miR-135b-5p was upregulated in bone tissue fragments of patients with osteoporosis compared with the control patients. MC3T3-E1 cells were used to perform osteogenic differentiation induction. Reverse transcription-quantitative PCR and western blot assay were used to detect the mRNA and protein expression levels of the osteogenic markers osteocalcin (OC), Osterix and alkaline phosphatase (ALP). A specific kit was used for detecting ALP activity. The present results indicated that the mRNA expression levels of OC, Osterix and ALP significantly increased on the 7 and 14th day after osteogenic differentiation induction compared with the control group. Protein expression levels of OC, Osterix and ALP also increased on the 7 and 14th day after induction. ALP assay showed that ALP activity was significantly increased on the 7 and 14th day after induction. In addition, the present study found that miR-135b-5p was downregulated in MC3T3-E1 cells 7 and 14 days after osteogenic differentiation induction. The results of TargetScan analysis and dual luciferase reporter gene assay indicated that runt-related transcription factor 2 (RUNX2) was a direct target gene of miR-135b-5p. RUNX2 was upregulated in MC3T3-E1 cells on the 7 and 14th day after induction. Moreover, the present study found that compared with the osteogenic differentiation induction group, miR-135b-5p mimic significantly decreased OC, Osterix and ALP expression, and reduced ALP activity in MC3T3-E1 cells. However, these reductions were reversed following overexpression of RUNX2. The present results showed that miR-135b-5p mimic significantly reduced cell viability in MC3T3-E1 cells and induced cell apoptosis, and these effects were significantly reversed following RUNX2 overexpression. In summary, the present results suggested that miR-135-5p participated in the occurrence and development of osteoporosis via inhibition of osteogenic differentiation and osteoblast growth by targeting RUNX2. The present study suggested a novel potential target that may faciliate the treatment of osteoporosis, and further study is required to examine this possibility.

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Section: Methodsmentioning

confidence: 99%

Abnormal expression of miR‑135b‑5p in bone tissue of patients with osteoporosis and its role and mechanism in osteoporosis progression

et al. 2019

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“…Liu et al (2018) Interestingly, in one study, miR-98-5p negatively regulated the expression of casein kinase 2 interacting protein-1 (CKIP-1) gene and protein to promote the osteogenic differentiation of MC3T3-E1 cells (Liu et al, 2018). But another study in three types of cells (MC3T3-E1 cells, mouse and human BMSCs), miR-98-5p inhibited osteogenic differentiation by targeting HMGA2 (Zheng et al, 2019). And for miR-224, it inhibited osteoblast differentiation in mesenchymal stem cells by directly targeting Smad4 (Luo et al, 2018), but miR-224 regulated the expression of Rac1 to promoted osteogenic differentiation in human mesenchymal stem cells (Cai et al, 2019).…”

Section: Mirnas Regulate Other Factors In Osteoblastsmentioning

confidence: 99%

Roles of MicroRNAs in Bone Destruction of Rheumatoid Arthritis

Zhao

2020

Front. Cell Dev. Biol.

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As an important pathological result of rheumatoid arthritis (RA), bone destruction will lead to joint injury and dysfunction. The imbalance of bone metabolism caused by increased osteoclast activities and decreased osteoblast activities is the main cause of bone destruction in RA. MicroRNAs (MiRNAs) play an important role in regulating bone metabolic network. Recent studies have shown that miRNAs play indispensable roles in the occurrence and development of bone-related diseases including RA. In this paper, the role of miRNAs in regulating bone destruction of RA in recent years, especially the differentiation and activities of osteoclast and osteoblast, is reviewed. Our results will not only help provide ideas for further studies on miRNAs' roles in regulating bone destruction, but give candidate targets for miRNAs-based drugs research in bone destruction therapy of RA as well.

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“…Furthermore, the expression of miR-98-5p was significantly upregulated in MC3T3-E1 cells following Kcnq1ot1 knockdown. miR-98-5p overexpression inhibits osteogenic differentiation and proliferation of MC3T3-E1 osteoblasts by targeting high mobility group AT-Hook2, thereby obstructing bone regeneration ( 20 ). In agreement with the aforementioned studies, miR-98-5p silencing rescued the inhibitory effect of Kcnq1ot1 knockdown on osteogenic differentiation and mineralization, suggesting that Kcnq1ot1 silencing may serve a suppressive role in bone formation by upregulating miR-98-5p expression.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, miR-98-5p has been reported to participate in myocardial differentiation of bone marrow mesenchymal stem cells via the regulation of T-box transcription factor 5 (Tbx5) ( 19 ). In addition, this miRNA may target high mobility group AT-hook 2 to inhibit the osteogenic differentiation of MC3T3-E1 osteoblasts, thereby obstructing bone regeneration ( 20 ). Thus, it was hypothesized that Kcnq1ot1 may affect osteogenic differentiation by binding to miR-98-5p.…”

Section: Introductionmentioning

confidence: 99%

lncRNA Kcnq1ot1 promotes bone formation by inhibiting miR‑98‑5p/Tbx5 axis in MC3T3‑E1 cells

2022

Self Cite

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Long non-coding (lnc)RNA KCNQ1 opposite strand/antisense transcript 1 (Kcnq1ot1) has been shown to regulate multiple biological processes. However, the functional role of Kcnq1ot1 in osteoporosis and the underlying mechanism are still unclear. The present study aimed to investigate the function of lncRNA Kcnq1ot1 in osteogenic differentiation. Alkaline phosphatase (ALP) activity was measured using an ALP assay kit. Western blotting was performed to assess the expression levels of osteogenic differentiation-associated proteins. Reverse transcription-quantitative PCR was performed to detect Kcnq1ot1, microRNA (miR)-98-5p and T-box transcription factor 5 (Tbx5) expression levels. The binding of Kcnq1ot1 with miR-98-5p and that of miR-98-5p with Tbx5 were predicted by starBase and TargetScan databases, respectively, and verified using dual luciferase reporter assays. The mineralization of MC3T3-E1 cells was observed using an Alizarin red S staining assay. The results revealed that expression of Kcnq1ot1 was increased and that of miR-98-5p was decreased during osteogenic differentiation. Additionally, Kcnq1ot1 was shown to target miR-98-5p and inhibit its expression. Inhibiting miR-98-5p reversed the inhibitory effect of Kcnq1ot1 knockdown on osteogenic differentiation and mineralization of MC3T3-E1 cells. Furthermore, Kcnq1ot1 regulated Tbx5 expression via miR-98-5p. Overexpressing miR-98-5p or downregulating Tbx5 expression reversed the promotive effect of Kcnq1ot1 overexpression on osteogenic differentiation and mineralization of MC3T3-E1 cells. In conclusion, these findings suggested that Kcnq1ot1 may promote bone formation by inhibiting miR-98-5p and upregulating Tbx5. Kcnq1ot1, miR-98-5p and Tbx5 may therefore serve as promising targets for the treatment of osteoporosis.

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MicroRNA‑98‑5p prevents bone regeneration by targeting high mobility group AT‑Hook 2

Cited by 9 publications

References 34 publications

Abnormal expression of miR‑135b‑5p in bone tissue of patients with osteoporosis and its role and mechanism in osteoporosis progression

Abnormal expression of miR‑135b‑5p in bone tissue of patients with osteoporosis and its role and mechanism in osteoporosis progression

Roles of MicroRNAs in Bone Destruction of Rheumatoid Arthritis

lncRNA Kcnq1ot1 promotes bone formation by inhibiting miR‑98‑5p/Tbx5 axis in MC3T3‑E1 cells

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