Evidence map›Paper›PMID 26247736›Full record

ArticleCell death & disease2015

MiR-26a functions oppositely in osteogenic differentiation of BMSCs and ADSCs depending on distinct activation and roles of Wnt and BMP signaling pathway.

X Su, L Liao, Y Shuai, H Jing, S Liu, H Zhou, Y Liu, Y Jin

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 143 citations in OpenAlex.

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  18. Differential circRNA and mRNA Expression Profiling During Osteogenic Differentiation in Rat Bone Marrow Mesenchymal Stem Cells.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Article
  19. Exosomal miRNAs from Prostate Cancer Impair Osteoblast Function in Mice.International journal of molecular sciences · 2022
    Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

X Su1] Department of Orthodontics, Stomatology Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710004, China [2] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [3] Institute of Neurobiology, Environment and Genes Related to Diseases, Key Laboratory of Education Ministry, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, China.
L Liao1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Xi'an, Shaanxi 710032, China [3] State Key Laboratory of Military Stomatology, Department of Oral Histology and pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Y Shuai1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Xi'an, Shaanxi 710032, China [3] State Key Laboratory of Military Stomatology, Department of Oral Histology and pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
H Jing1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Xi'an, Shaanxi 710032, China [3] State Key Laboratory of Military Stomatology, Department of Oral Histology and pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
S Liu1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Xi'an, Shaanxi 710032, China [3] State Key Laboratory of Military Stomatology, Department of Oral Histology and pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
H ZhouDepartment of Orthodontics, Stomatology Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710004, China.
Y LiuInstitute of Neurobiology, Environment and Genes Related to Diseases, Key Laboratory of Education Ministry, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, China.
Y Jin1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Xi'an, Shaanxi 710032, China.
Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) emerge as important regulators of stem cell lineage commitment and bone development. MiRNA-26a (miR-26a) is one of the important miRNAs regulating osteogenic differentiation of both bone marrow-derived mesenchymal stem cells (BMSCs) and adipose tissue-derived mesenchymal stem cells (ADSCs). However, miR-26a functions oppositely in osteogenic differentiation of BMSCs and ADSCs, suggesting distinct post-transcriptional regulation of tissue-specific MSC differentiation. However, the molecular basis is largely unknown. Here, we report that the function of miR-26a is largely depended on the intrinsic signaling regulation network of MSCs. Using bioinformatics and functional assay, we confirmed that miR-26a potentially targeted on GSK3β and Smad1 to regulate Wnt and BMP signaling pathway. Overall comparative analysis revealed that Wnt signaling was enhanced more potently and played a more important role than BMP signaling in osteogenic differentiation of BMSCs, whereas BMP pathway was more essential for promoting osteogenic differentiation of ADSCs. The distinct activation pattern and role of signaling pathways determined that miR-26a majorly targeted on GSK3β to activate Wnt signaling for promoting osteogenic differentiation of BMSCs, whereas it inhibited Smad1 to suppress BMP signaling for interfering with the osteogenic differentiation of ADSCs. Taken together, our study demonstrated that BMSCs and ADSCs applied different signaling pathway to facilitate their osteogenic differentiation, which determined the inverse function of miR-26a. The distinct transcriptional regulation and post-transcriptional regulation network suggested the intrinsic molecular differences between tissue-specific MSCs and the complexity in MSC research and MSC-based cell therapy.

Indexed as

Adipose TissueAnimalsBone Marrow CellsBone Morphogenetic Protein ReceptorsCell DifferentiationGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMesenchymal Stem CellsMiceMice, Inbred BALB CMice, Inbred C57BLMice, NudeMicroRNAsOrgan SpecificityOsteogenesisBone Morphogenetic Protein ReceptorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseMicroRNAsMirn26 microRNA, mouseSmad1 ProteinSmad1 protein, mouse

Identifiers

PMID26247736
PMCPMC4558512
OpenAlexW962052387

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.