Evidence map›Paper›PMID 25428397›Full record

ArticleScientific reports2014

Licochalcone A up-regulates of FasL in mesenchymal stem cells to strengthen bone formation and increase bone mass.

Leiguo Ming, Fang Jin, Ping Huang, Hailang Luo, Wenjia Liu, Leilei Zhang, Wei Yuan, Yongjie Zhang, Yan Jin

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.1field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

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  6. Necroptosis in pathogenesis of osteoarthritis and its therapeutic implications.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
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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

9 authors at 1 institution in 1 country.

Leiguo Ming1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] State Key Laboratory of Military Stomatology, Department of Oral Histology and Pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [3] Institute forTissue Engineering and Regenerative Medicine Research of Xi'an, Xi'an, China.
Fang JinDepartment of Orthodontics, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi, China.
Ping HuangDepartment of Clinical Laboratory, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi. 710032, China.
Hailang Luo1] State Key Laboratory of Military Stomatology, Department of Oral Histology and Pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Institute forTissue Engineering and Regenerative Medicine Research of Xi'an, Xi'an, China.
Wenjia Liu1] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] State Key Laboratory of Military Stomatology, Department of Oral Histology and Pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [3] Institute forTissue Engineering and Regenerative Medicine Research of Xi'an, Xi'an, China.
Leilei Zhang1] State Key Laboratory of Military Stomatology, Department of Oral Histology and Pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Institute forTissue Engineering and Regenerative Medicine Research of Xi'an, Xi'an, China.
Wei Yuan1] State Key Laboratory of Military Stomatology, Department of Oral Histology and Pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Institute forTissue Engineering and Regenerative Medicine Research of Xi'an, Xi'an, China.
Yongjie Zhang1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, 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.
Yan Jin1] State Key Laboratory of Military Stomatology, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, China [2] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Shaanxi 710032, China [3] Institute forTissue Engineering and Regenerative Medicine Research of Xi'an, Xi'an, China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of bone marrow-derived mesenchymal stem cells(BMSCs)in the pathogenesis and therapy of osteoporosis has drawn increasing attention in recent years. In the development of osteoporosis, it has been demonstrated that many changes occurred in the behavior of BMSCs. For example, the biological system of FasL pathways mediated differentiation of ERK and GSK-3β-catenin pathway was damaged. Here we found that 0.35 mg/L Licochalcone A (L-A) had a strong effect in increasing the osteogenic differentiation and mineralization of BMSCs both in vivo and in vitro by up-regulating FasL and further playing a role in regulating the ERK and GSK-3β-catenin systems. It has also demonstrated that the administration of L-A could restore the biological function of the damaged BMSCs differentiation by recovering or protecting bone mass in a disease state through activating the endosteal bone formation and partially inhibiting bone resorption in acute estrogen deficiency model. Results of our study suggested that careful titration of MSC was response to L-A and up-regulated FasL pathways mediating differentiation of ERK and GSK-3β-catenin biological systems under disease state in vivo, restore the impaired function, is one of the ways of L-A relieve or treatment osteoporosis.

Indexed as

AnimalsBone and BonesCell DifferentiationCells, CulturedChalconesFas Ligand ProteinFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMAP Kinase Signaling SystemMesenchymal Stem CellsOsteogenesisRatsRats, Sprague-DawleyUp-RegulationChalconesFaslg protein, ratFas Ligand ProteinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratlicochalcone A

Identifiers

PMID25428397
PMCPMC4245531
OpenAlexW1965647381

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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.