Evidence map›Paper›PMID 29372627›Full record

ArticleJournal of cellular and molecular medicine2018

Leptin regulates disc cartilage endplate degeneration and ossification through activation of the MAPK-ERK signalling pathway in vivo and in vitro.

Ying-Chao Han, Bin Ma, Song Guo, Mingjie Yang, Li-Jun Li, Shan-Jin Wang, Jun Tan

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 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

7 authors at 1 institution in 1 country.

Ying-Chao HanDepartment of Orthopedics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Bin MaDepartment of Orthopedics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Song GuoDepartment of Orthopedics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Mingjie YangDepartment of Orthopedics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Li-Jun LiDepartment of Orthopedics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shan-Jin WangDepartment of Spinal Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0001-7164-5904
Jun TanDepartment of Orthopedics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent findings demonstrate that leptin plays a significant role in chondrocyte and osteoblast differentiation. However, the mechanisms by which leptin acts on cartilage endplate (CEP) cells to give rise to calcification are still unclear. The aim of this study was to evaluate the effects of leptin that induced mineralization of CEP cells in vitro and in vivo. We constructed a rat model of lumbar disc degeneration and determined that leptin was highly expressed in the presence of CEP calcification. Rat CEP cells treated with or without leptin were used for in vitro analysis using RT-PCR and Western blotting to examine the expression of osteocalcin (OCN) and runt-related transcription factor 2 (Runx2). Both OCN and Runx2 expression levels were significantly increased in a dose- and time-dependent manner. Leptin activated ERK1/2 and STAT3 phosphorylation in a time-dependent manner. Inhibition of phosphorylated ERK1/2 using targeted siRNA suppressed leptin-induced OCN and Runx2 expression and blocked the formation of mineralized nodules in CEP cells. We further demonstrated that exogenous leptin induced matrix mineralization of CEP cells in vivo. We suggest that leptin promotes the osteoblastic differentiation of CEP cells via the MAPK/ERK signal transduction pathway and may be used to investigate the mechanisms of disc degeneration.

Indexed as

MAP Kinase Signaling SystemAnimalsCalcification, PhysiologicCartilageCell DifferentiationCore Binding Factor Alpha 1 SubunitDisease Models, AnimalIntervertebral Disc DegenerationLeptinLumbar VertebraeMaleMotor EndplateOsteocalcinOsteogenesisPhosphorylationRats, Sprague-DawleyCore Binding Factor Alpha 1 SubunitLeptinOsteocalcinSTAT3 Transcription FactorCalcificationCartilage endplateLeptinMAPKSTAT3

Identifiers

PMID29372627
PMCPMC5867127
OpenAlexW2790214241

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.