Evidence map›Paper›PMID 31742919›Full record

ArticleStem cells translational medicine2020

Neural cell adhesion molecule regulates chondrocyte hypertrophy in chondrogenic differentiation and experimental osteoarthritis.

Bin-Feng Cheng, Jun-Jiang Lian, Hai-Jie Yang, Lei Wang, Hao-Heng Yu, Jia-Jia Bi, Yao-Xin Gao, Su-Juan Chen, Mian Wang, Zhi-Wei Feng

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Bin-Feng ChengSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.ORCID 0000-0002-4742-1748
Jun-Jiang LianSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Hai-Jie YangSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Lei WangSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Hao-Heng YuHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Jia-Jia BiSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Yao-Xin GaoSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Su-Juan ChenSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Mian WangSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Zhi-Wei FengSchool of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Xinxiang Medical University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondrocyte hypertrophy-like change is an important pathological process of osteoarthritis (OA), but the mechanism remains largely unknown. Neural cell adhesion molecule (NCAM) is highly expressed and involved in the chondrocyte differentiation of mesenchymal stem cells (MSCs). In this study, we found that NCAM deficiency accelerates chondrocyte hypertrophy in articular cartilage and growth plate of OA mice. NCAM deficiency leads to hypertrophic chondrocyte differentiation in both murine MSCs and chondrogenic cells, in which extracellular signal-regulated kinase (ERK) signaling plays an important role. Moreover, NCAM expression is downregulated in an interleukin-1β-stimulated OA cellular model and monosodium iodoacetate-induced OA rats. Overexpression of NCAM substantially inhibits hypertrophic differentiation in the OA cellular model. In conclusion, NCAM could inhibit hypertrophic chondrocyte differentiation of MSCs by inhibiting ERK signaling and reduce chondrocyte hypertrophy in experimental OA model, suggesting the potential utility of NCAM as a novel therapeutic target for alleviating chondrocyte hypertrophy of OA.

Indexed as

AnimalsCell DifferentiationChondrocytesChondrogenesisHumansMiceNeural Cell Adhesion MoleculesOsteoarthritisRatsRats, WistarTransfectionNeural Cell Adhesion Moleculeschondrocyte differentiationchondrocyte hypertrophymesenchymal stem cellsNCAMosteoarthritis

Identifiers

PMID31742919
PMCPMC6988767
OpenAlexW2991277901

What OpenQuestion holds

Textmetadata
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.