Evidence map›Paper›PMID 34419165›Full record

ArticleStem cell research & therapy2021

Melatonin contributes to the hypertrophic differentiation of mesenchymal stem cell-derived chondrocytes via activation of the Wnt/β-catenin signaling pathway : Melatonin promotes MSC-derived chondrocytes hypertrophy.

Xuan Wang, Tianwei He, Lei He, Bu Yang, Zhongyu Liu, Mao Pang, Peigen Xie, Liangming Zhang, Limin Rong

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  13. Melatonin and the Programming of Stem Cells.International journal of molecular sciences · 2022
    Review
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  16. CaIn vivo (Athens, Greece)
    Article
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.

Xuan Wang *Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Tianwei He *Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Lei He *Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Bu YangDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Zhongyu LiuDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Mao PangDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Peigen XieDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Liangming ZhangDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China. zhanglm36@mail.sysu.edu.cn.
Limin RongDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China. ronglm@mail.sysu.edu.cn.ORCID 0000-0002-4049-870X
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertrophy is a critical process for chondrocyte differentiation and maturation during endochondral ossification, which is responsible for the formation of long bone and postnatal longitudinal growth. Increasing evidence suggests that melatonin, an indole hormone, plays a pivotal role in chondrogenesis. However, little is known about the effects of melatonin on the terminal differentiation of chondrocytes.

methodsMesenchymal stem cell (MSC)-derived chondrocytes generated by a high-density micromass culture system were induced to undergo hypertrophic differentiation. Melatonin-mediated hypertrophic differentiation was examined by reverse transcription polymerase chain reaction analysis (RT-PCR) analysis, histological staining and immunohistochemistry. Activation of the Wnt signaling pathway was evaluated by PCR array, RT-PCR, western blotting and immunofluorescence. XAV-939, a Wnt signaling pathway antagonist, was further used to determine whether the effect of melatonin on chondrocyte hypertrophic differentiation was mediated occurred by activation of Wnt signaling pathway.

resultsHistological staining showed melatonin increased chondrocyte cell volume and the expression of type X collagen but decreased the expression of type II collagen compared with the control group. RT-PCR showed that melatonin significantly up-regulated the gene expressions of biomarkers of hypertrophic chondrocytes, including type X collagen, alkaline phosphatase, runt-related transcription factor 2, Indian hedgehog and parathyroid hormone-related protein receptor, and melatonin down-regulated the mRNA expression of hallmarks of chondrocytes, including parathyroid hormone-related protein. PCR array showed that the effect of melatonin on chondrocyte hypertrophic differentiation was accompanied by the up-regulation of multiple target genes of the canonical Wnt signaling pathway, and this effect was blocked by XAV-939.

conclusionsThe current findings demonstrate that melatonin enhances the hypertrophic differentiation of MSC-derived chondrocytes through the Wnt signaling pathway. Our findings add evidence to the role of melatonin in promoting bone development and highlight the positive effects of melatonin on terminal differentiation of chondrocytes.

Indexed as

MelatoninMesenchymal Stem CellsCell DifferentiationCells, CulturedChondrocytesChondrogenesisHedgehog ProteinsHumansHypertrophyWnt ProteinsWnt Signaling PathwayHedgehog ProteinsMelatoninWnt ProteinsChondrocyte hypertrophyMelatoninMesenchymal stem cellsWnt/β-catenin

Identifiers

PMID34419165
PMCPMC8379782
OpenAlexW3195066875

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.