Evidence map›Paper›PMID 26538836›Full record

ArticleMediators of inflammation2015

Protein Phosphatase 2A Mediates Oxidative Stress Induced Apoptosis in Osteoblasts.

Chong-xin Huang, Bo Lv, Yue Wang

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

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  12. An overview of the role of lipid peroxidation-derived 4-hydroxynonenal in osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
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  15. Dexmedetomidine attenuates HJournal of dental anesthesia and pain medicine · 2016
    Article
  16. Deletion of Pr130 Interrupts Cardiac Development in Zebrafish.International journal of molecular sciences · 2016
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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

3 authors at 1 institution in 1 country.

Chong-xin HuangDepartment of Orthopaedics, Sichuan Provincial People's Hospital, No. 32 West Second Section, First Ring Road, Chengdu 610072, China.
Bo LvDepartment of Orthopaedics, Sichuan Provincial People's Hospital, No. 32 West Second Section, First Ring Road, Chengdu 610072, China.
Yue WangDepartment of Orthopaedics, Sichuan Provincial People's Hospital, No. 32 West Second Section, First Ring Road, Chengdu 610072, China.
Chengdu Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is one of the most common bone diseases, which is characterized by a systemic impairment of bone mass and fragility fractures. Age-related oxidative stress is highly associated with impaired osteoblastic dysfunctions and subsequent osteoporosis. In osteoblasts (bone formation cells), reactive oxygen species (ROS) are continuously generated and further cause lipid peroxidation, protein damage, and DNA lesions, leading to osteoblastic dysfunctions, dysdifferentiations, and apoptosis. Although much progress has been made, the mechanism responsible for oxidative stress induced cellular alternations and osteoblastic toxicity is still not fully elucidated. Here, we demonstrate that protein phosphatase 2A (PP2A), a major protein phosphatase in mammalian cells, mediates oxidative stress induced apoptosis in osteoblasts. Our results showed that lipid peroxidation products (4-HNE) may induce dramatic oxidative stress, inflammatory reactions, and apoptosis in osteoblasts. These oxidative stress responses may ectopically activate PP2A phosphatase activity, which may be mediated by inactivation of AKT/mTOR pathway. Moreover, inhibition of PP2A activity by okadaic acid might partly prevent osteoblastic apoptosis under oxidative conditions. These findings may reveal a novel mechanism to clarify the role of oxidative stress for osteoblastic apoptosis and provide new possibilities for the treatment of related bone diseases, such as osteoporosis.

Indexed as

ApoptosisOxidative StressAldehydesAnimalsAnimals, NewbornBone RemodelingInflammationLipid PeroxidationMiceOkadaic AcidOsteoblastsOsteoporosisProtein Phosphatase 2Proto-Oncogene Proteins c-aktReactive Oxygen SpeciesReal-Time Polymerase Chain Reaction4-hydroxy-2-nonenalAkt1 protein, mouseAldehydesOkadaic AcidProtein Phosphatase 2Proto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID26538836
PMCPMC4619977
OpenAlexW1963173014

What OpenQuestion holds

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LicenceCC BY
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.