Evidence map›Paper›PMID 27806136›Full record

ArticlePloS one2016

Cyclic Compressive Stress Regulates Apoptosis in Rat Osteoblasts: Involvement of PI3K/Akt and JNK MAPK Signaling Pathways.

Fanglong Song, Yi Wang, Dawei Jiang, Tianchen Wang, Yinquan Zhang, Hui Ma, Yifan Kang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 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.

Fanglong SongDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.
Yi WangDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.
Dawei JiangDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.
Tianchen WangDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.
Yinquan ZhangDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.
Hui MaDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.
Yifan KangDepartment of Orthopedics, Third Affiliated Hospital of PLA Second Military Medical University, Shanghai, 200433, China.ORCID http://orcid.org/0000-0002-5856-6643
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is widely accepted that physiological mechanical stimulation suppresses apoptosis and induces synthesis of extracellular matrix by osteoblasts; however, the effect of stress overloading on osteoblasts has not been fully illustrated. In the present study, we investigated the effect of cyclic compressive stress on rat osteoblasts apoptosis, using a novel liquid drop method to generate mechanical stress on osteoblast monolayers. After treatment with different levels of mechanical stress, apoptosis of osteoblasts and activations of mitogen-activated protein kinases (MAPKs) and PI3-kinase (PI3K)/Akt signaling pathways were investigated. Osteoblasts apoptosis was observed after treated with specific inhibitors prior to mechanical stimulation. Protein levels of Bax/Bcl-2/caspase-3 signaling were determined using western blot with or without inhibitors of PI3K/Akt and phosphorylation of c-jun N-terminal kinase (JNK) MAPK. Results showed that mechanical stimulation led to osteoblasts apoptosis in a dose-dependent manner and a remarkable activation of MAPKs and PI3K/Akt signaling pathways. Activation of PI3K/Akt protected against apoptosis, whereas JNK MAPK increased apoptosis via regulation of Bax/Bcl-2/caspase-3 activation. In summary, the PI3K/Akt and JNK MAPK signaling pathways played opposing roles in osteoblasts apoptosis, resulting in inhibition of apoptosis upon small-magnitude stress and increased apoptosis upon large-magnitude stress.

Indexed as

MAP Kinase Signaling SystemStress, MechanicalAnimalsApoptosisCaspase 3Cell Culture TechniquesCell Line, TumorCell SurvivalOsteoblastsPhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-aktRatsCasp3 protein, ratCaspase 3Phosphatidylinositol 3-KinaseProto-Oncogene Proteins c-akt

Identifiers

PMID27806136
PMCPMC5091858
OpenAlexW2548979602

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.