Evidence map›Paper›PMID 27127181›Full record

ArticleOncotarget2016

Glucocorticoid impairs cell-cell communication by autophagy-mediated degradation of connexin 43 in osteocytes.

Junjie Gao, Tak Sum Cheng, An Qin, Nathan J Pavlos, Tao Wang, Kai Song, Yan Wang, Lianzhi Chen, Lin Zhou, Qing Jiang and 3 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 57 citations in OpenAlex.

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  17. Pulsed electromagnetic fields: promising treatment for osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2019
    Review
  18. Article
  19. Article
  20. Autophagy as a target for glucocorticoid-induced osteoporosis therapy.Cellular and molecular life sciences : CMLS · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 8 institutions in 3 countries.

Junjie GaoCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
Tak Sum ChengCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
An QinShanghai Key Laboratory of Orthopedic Implants, Department of Orthopedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nathan J PavlosCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
Tao WangCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
Kai SongCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
Yan WangKey Laboratory of Combined Muti-Organ Transplantation, Ministry of Public Health, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Division of Hepatobiliary Pancreatic Surgery, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lianzhi ChenCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
Lin ZhouKey Laboratory of Combined Muti-Organ Transplantation, Ministry of Public Health, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Division of Hepatobiliary Pancreatic Surgery, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Qing JiangDepartment of Sports Medicine and Adult Reconstruction Surgery, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, Jiangsu, China.
Hiroshi TakayanagiCentre for Orthopaedic Research, School of Surgery, The University of Western Australia, Nedlands, Western Australia, Australia.
Sheng YanState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Minghao ZhengState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
University of Western Australia · AUState Key Laboratory of Diagnosis and Treatment of Infectious DiseasesFirst Affiliated Hospital Zhejiang University · CNGuangdong Academy of Medical Sciences · CNNanjing Drum Tower Hospital · CNShanghai Jiao Tong University · CNThe University of Tokyo · JPZhejiang University · CN

Funding

EtOH Modulation of Synaptic Plasticity in Nucleus AccumbensR01AA020501 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARTIN, GILLES E · 2012 to 2016
$1.6M
NIAAA NIH HHS R01 AA020501
6 · The paper itself

Abstract

Osteocytes comprising over 90% of the bone cell population are highly susceptible to the adverse effects of glucocorticoids (GC) administration. Here we observed that Dexamethasone (Dex) induces a robust cytoskeleton rearrangement and decreases Cx43 protein expression in osteocyte-like MLO-Y4 cells. Using a Dmp1Cre-mT/mG osteocyte ex vivo culture system, we found significant shortening of dendritic processes in primary osteocytes following Dex administration. Loss of dendritic processes is a consequence of reduced Cx43 connectivity upon Dex induced autophagy in both RFP-GFP-LC3B transfected MLO-Y4 cells and primary calvarial osteocytes from LC3GFP transgenic mice. Upon the induction of autophagy by Dex, Cx43 was internalized into autophagosome/autolysosomes and degraded by autophagy. The degradation was attenuated following lysosomal inhibition using chloroquine (CLQ) and suppression of autophagy by Atg5 silencing. Inhibition Akt-mTORC1 signaling by Dex induces autophagy subsequently resulting in Cx43 degradation.Activation of Akt phosphorylation by IGF-1 attenuated Dex induced autophagy and degradation of Cx43. Together, we demonstrated that GC impair osteocyte cell-cell connectivity via autophagy mediated degradation of Cx43 through inhibition of the Akt-mTORC1 signaling. This may account for the deleterious effect of GC-induced bone loss.

Indexed as

AnimalsAutophagosomesAutophagyBlotting, WesternCell CommunicationCell LineCells, CulturedConnexin 43DexamethasoneGlucocorticoidsLysosomesMice, TransgenicMicroscopy, ConfocalOsteocytesProteolysisSignal TransductionConnexin 43DexamethasoneGJA1 protein, mouseGlucocorticoidsautophagyconnexin 43GerotargetglucocorticoidmTORC1osteocyte

Identifiers

PMID27127181
PMCPMC5053625
OpenAlexW2344432847

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.