miR-33-5p, a novel mechano-sensitive microRNA promotes osteoblast differentiation by targeting Hmga2

Wang, Han; Sun, Zhongyang; Wang, Yixuan; Hu, Zebing; Zhou, Hua; Zhang, Lianchang; Hong, Bo; Zhang, Shu; Cao, Xinsheng

doi:10.1038/srep23170

Cited by 79 publications

(80 citation statements)

References 68 publications

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“…In particular, HMGA2 was a concern among those potential targets, as it has been reported that miR-33-5p promotes osteoblast differentiation by targeting HMGA2 [20]. Also, HMGA2 is associated with highly proliferating human bone marrow-derived mesenchymal stem cells and plays a role in bone formation [21].…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-495 Inhibits New Bone Regeneration via Targeting High Mobility Group AT-Hook 2 (HMGA2)

Tian

Zhou

et al. 2017

Med Sci Monit

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BackgroundMicroRNAs play critical roles in post-translational gene expression. In this study, we explored the role of miR-495 in new bone regeneration.Material/MethodsMurine calvarial osteoblasts were isolated and cultured. Microarray was performed to identify differential miRNAs in medicarpin-induced osteoblasts differentiation. Luciferase reporter assay was performed to identify the target gene of miRNA. Murine osteoblast cells were transfected with miC, miR-495, or anti-miR-495. CCK-8 and flow cytometry were performed to detect osteoblasts proliferation and apoptosis. Western blot was used to analyze apoptosis-related proteins. qRT-PCR analysis was performed to detect gene expression. ALP activity and mineralized nodule formation test were used to evaluate bone formation. Dill-hole injury model was constructed and micro CT was utilized to measuring bone healing.ResultsMicroarray analysis identified miR-495 as our miRNA of interest and luciferase reporter assay identified HMGA2 as its target gene. Over-expression of miR-495 significantly inhibited ALP activity and mineralized nodule formation as well as the expression of RUNX-2, BMP-2, and Osterix. Also, miR-495 over-expression inhibited osteoblasts proliferation and promoted apoptosis obviously. In this in vivo study, the downregulation of miR-495 promoted murine femur healing.ConclusionsMiR-495 inhibits new bone regeneration via targeting high mobility group AT-Hook 2 (HMGA2). We propose that targeting miR-495 may be a promising therapeutic approach for bone regeneration.

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Section: Resultsmentioning

confidence: 99%

MicroRNA-495 Inhibits New Bone Regeneration via Targeting High Mobility Group AT-Hook 2 (HMGA2)

Tian

Zhou

et al. 2017

Med Sci Monit

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“…36,38,39 To confirm the microgravity achieved by this clinostat, we tested the effects of the simulated microgravity on biological characteristics of primary mouse osteoblasts in this experimental condition ( Figure S1). The clinostat (Astronaut Research and Training Center, China) is an effective tool to simulate microgravity.…”

Section: Clinorotation To Simulate Microgravitymentioning

confidence: 99%

“…The chambers were divided into two groups: horizontal rotation control and clinorotation. 36,38,39 To confirm the microgravity achieved by this clinostat, we tested the effects of the simulated microgravity on biological characteristics of primary mouse osteoblasts in this experimental condition ( Figure S1).…”

Section: Clinorotation To Simulate Microgravitymentioning

confidence: 99%

miR‐181c‐5p mediates simulated microgravity‐induced impaired osteoblast proliferation by promoting cell cycle arrested in the G₂ phase

Sun

Liu

Wang

et al. 2019

J Cellular Molecular Medi

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Impaired osteoblast proliferation plays fundamental roles in microgravity‐induced bone loss, and cell cycle imbalance may result in abnormal osteoblast proliferation. However, whether microgravity exerts an influence on the cell cycle in osteoblasts or what mechanisms may underlie such an effect remains to be fully elucidated. Herein, we confirmed that simulated microgravity inhibits osteoblast proliferation. Then, we investigated the effect of mechanical unloading on the osteoblast cell cycle and found that simulated microgravity arrested the osteoblast cell cycle in the G 2 phase. In addition, our data showed that cell cycle arrest in osteoblasts from simulated microgravity was mainly because of decreased cyclin B1 expression. Furthermore, miR‐181c‐5p directly inhibited cyclin B1 protein translation by binding to a target site in the 3′UTR. Lastly, we demonstrated that inhibition of miR‐181c‐5p partially counteracted cell cycle arrest and decreased the osteoblast proliferation induced by simulated microgravity. In conclusion, our study demonstrates that simulated microgravity inhibits cell proliferation and induces cell cycle arrest in the G 2 phase in primary mouse osteoblasts partially through the miR‐181c‐5p/cyclin B1 pathway. This work may provide a novel mechanism of microgravity‐induced detrimental effects on osteoblasts and offer a new avenue to further investigate bone loss induced by mechanical unloading.

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“…It was also shown that miR‐133a could hamper bone formation by targeting RUNX2 . MiR‐33, on the other hand, was involved in mechano‐induced osteoblast differentiation, but its association with BMD has yet to be reported.…”

Section: Mirnas In Antiosteoporosis Treatmentmentioning

confidence: 99%

MicroRNA and Human Bone Health

Cheng

Tan

et al. 2018

JBMR Plus

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The small non‐coding microRNAs (miRNAs) are post‐transcription regulators that modulate diverse cellular process in bone cells. Because optimal miRNA targeting is essential for their function, single‐nucleotide polymorphisms (SNPs) within or proximal to the loci of miRNA (miR‐SNPs) or mRNA (PolymiRTS) could potentially disrupt the miRNA‐mRNA interaction, leading to changes in bone metabolism and osteoporosis. Recent human studies of skeletal traits using miRNA profiling, genomewide association studies, and functional studies started to decipher the complex miRNA regulatory network. These studies have indicated that miRNAs may be a promising bone marker. This review focuses on human miRNA studies on bone traits and discusses how genetic variants affect bone metabolic pathways. Major ex vivo investigations using human samples supported with animal and in vitro models have shed light on the mechanistic role of miRNAs. Furthermore, studying the miRNAs’ signatures in secondary osteoporosis and osteoporotic medications such as teriparatide (TPTD) and denosumab (DMab) have provided valuable insight into clinical management of the disease. © 2018 The Authors. JBMR Plus Published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research

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miR-33-5p, a novel mechano-sensitive microRNA promotes osteoblast differentiation by targeting Hmga2

Cited by 79 publications

References 68 publications

MicroRNA-495 Inhibits New Bone Regeneration via Targeting High Mobility Group AT-Hook 2 (HMGA2)

MicroRNA-495 Inhibits New Bone Regeneration via Targeting High Mobility Group AT-Hook 2 (HMGA2)

miR‐181c‐5p mediates simulated microgravity‐induced impaired osteoblast proliferation by promoting cell cycle arrested in the G₂ phase

MicroRNA and Human Bone Health

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miR-33-5p, a novel mechano-sensitive microRNA promotes osteoblast differentiation by targeting Hmga2

Cited by 79 publications

References 68 publications

MicroRNA-495 Inhibits New Bone Regeneration via Targeting High Mobility Group AT-Hook 2 (HMGA2)

MicroRNA-495 Inhibits New Bone Regeneration via Targeting High Mobility Group AT-Hook 2 (HMGA2)

miR‐181c‐5p mediates simulated microgravity‐induced impaired osteoblast proliferation by promoting cell cycle arrested in the G2 phase

MicroRNA and Human Bone Health

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miR‐181c‐5p mediates simulated microgravity‐induced impaired osteoblast proliferation by promoting cell cycle arrested in the G₂ phase