Evidence map›Paper›PMID 29393368›Full record

ArticleInternational journal of molecular medicine2018

Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells.

Wanlin Liu, Zhenqun Zhao, Yuyan Na, Chenyang Meng, Jianzhong Wang, Rui Bai

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 74 citations in OpenAlex.

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  14. International journal of molecular sciences · 2023
    Article
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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

6 authors at 1 institution in 1 country.

Wanlin LiuDepartment of Pediatric Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010030, P.R. China.
Zhenqun ZhaoDepartment of Pediatric Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010030, P.R. China.
Yuyan NaDepartment of Pediatric Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010030, P.R. China.
Chenyang MengDepartment of Pediatric Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010030, P.R. China.
Jianzhong WangDepartment of Orthopedics and Trauma, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010030, P.R. China.
Rui BaiDepartment of Pediatric Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010030, P.R. China.
Second Affiliated Hospital of Inner Mongolia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis of osteoblasts, triggered by prolonged or excessive use of glucocorticoids (GCs), has been identified as a dominant contributor to the development of osteoporosis and osteonecrosis. However, the molecular mechanisms underlying GC‑induced apoptosis are multifaceted and remain to be fully elucidated. The present study aimed to explore the correlation between dexamethasone (DEX)‑induced reactive oxygen species (ROS), autophagy and apoptosis in MC3T3‑E1 osteoblast‑like cells. Cell viability was assessed using a Cell Counting Kit‑8 assay, and flow cytometry was performed to assess cellular apoptosis, cell cycle and ROS production. Immunofluorescence and western blot analysis were respectively used to detect autophagic vacuoles and the expression of proteins, including cyclin D kinase (CDK)2, poly[ADP ribose] polymerase, caspase‑3, activating transcription factor (ATF)4, CCAAT/enhancer‑binding protein homologous protein (CHOP), Beclin1, microtubule‑associated proteins 1A/1B light chain (LC)3B and P62. It was revealed that DEX not only reduced cell viability, but also promoted apoptosis via the activation of endoplasmic reticulum (ER) stress. In addition, DEX induced cell cycle arrest at G0/G1 phase via inhibition of the expression of CDK2, and the production of ROS was activated. Of note, the DEX‑mediated changes in viability and apoptosis were attenuated in MC3T3‑E1 cells after treatment with 3‑methyladenine, which is an autophagy inhibitor. Treatment with the antioxidant N‑acetylcysteine abolished the effect of DEX on the proliferation, apoptosis, ER stress and autophagy of MC3T3‑E1 cells. In conclusion, the present results indicated that DEX promoted the production of ROS, which enhanced apoptosis through activation of autophagy and ER stress in MC3T3-E1 cells.

Indexed as

AnimalsApoptosisAutophagyCell LineCell SurvivalDexamethasoneEndoplasmic Reticulum StressGlucocorticoidsMiceOsteoblastsReactive Oxygen SpeciesDexamethasoneGlucocorticoidsReactive Oxygen Species

Identifiers

PMID29393368
PMCPMC5810234
OpenAlexW2788029357

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.