Evidence map›Paper›PMID 31966708›Full record

ArticleInternational journal of clinical and experimental pathology2017

Leptin inhibits AMPKα2 down-regulation induced decrease in the osteocytic MLO-Y4 cell proliferation and the expression of osteogenic markers.

Qing Fan, Hao Li, Zhu Liu, Zhiqiang Zhang, Hai Li, Jing Ding, Ziming Zhang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Metformin and bone metabolism: unraveling their direct and indirect effects.Therapeutic advances in endocrinology and metabolism · 2025
    Review
  2. Review
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.

Qing FanDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
Hao LiDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
Zhu LiuDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
Zhiqiang ZhangDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
Hai LiDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
Jing DingDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
Ziming ZhangDepartment of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, P. R. China.
XinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) is of biological and clinical importance for regulating cellular and systemic energy homeostasis. Although AMPKα1, one of the two AMPK's catalytic subunit α, expresses in the bone and stimulates bone nodule formation, the role of AMPKα2 in osteogenesis remains incompletely understood. The aim of this study was to determine the role of AMPKα2 in osteocytic MLO-Y4 cellproliferation and the expression of osteogenic markers. The current study silenced AMPKα2 in MLO-Y4 cells by transfection with pLKO.1-AMPKα2-shRNA vector and analyzed cell proliferation and the expression of osteogenic markers in MLO-Y4 cells with or without 100 μg/ml leptin treatment through CCK-8, Real-time PCR, Western blot and RNA-seq assay. We found that knockdown of AMPKα2 significantly decreased the mRNA level of AMPKα2 and the cell proliferation of MLO-Y4 cellsas well as the mRNA and protein levels of OPG, OCN, OPN, ALP and BMP6 and the protein expression of p-Smad5/Smad5. However, leptin treatment increased the MLO-Y4 cell proliferation and the expression of these osteogenic markers in MLO-Y4 cells with or without AMPKα2 silencing. Furthermore, RNA-seq assay showed 1019 transcriptors decreased in AMPKα2-silencing group and 995 transcriptors increased in leptin group compared with control group, respectively. 737 transcriptors decreased in AMPKα2-silencing group and 1282 transcriptors increased inleptin group compared with AMPKα2-silencing+leptin group, respectively. These findings suggest that AMPKα2 knockdown inhibited MLO-Y4 cell proliferation and osteogenic marker expressions, which implicates an important role of AMPKα2 in osteogenesis

Indexed as

AMPKα2GSEAleptinosteogenesisRNA-seq

Identifiers

PMID31966708
PMCPMC6965451
OpenAlexW2909706286

What Socratic holds

Textmetadata
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 Socratic graph.