Evidence map›Paper›PMID 20051625›Full record

ArticleThe Journal of clinical investigation2010

Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice.

Emma C Walker, Narelle E McGregor, Ingrid J Poulton, Melissa Solano, Sueli Pompolo, Tania J Fernandes, Matthew J Constable, Geoff C Nicholson, Jian-Guo Zhang, Nicos A Nicola and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

148 citing papers in PubMed, 298 citations in OpenAlex.

  1. Review
  2. Review
  3. Human germline biallelic loss-of-functionJournal of human immunity · 2026
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  16. Isolation, Purification, Generation, and Culture of Osteocytes.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Article

88 more citing papers are in PubMed but not listed here.

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

13 authors at 5 institutions in 2 countries.

Emma C WalkerSt. Vincent's Institute, Victoria, Australia.
Narelle E McGregor
Ingrid J Poulton
Melissa Solano
Sueli Pompolo
Tania J Fernandes
Matthew J Constable
Geoff C Nicholson
Jian-Guo Zhang
Nicos A Nicola
Matthew T Gillespie
T John Martin
Natalie A Sims
St Vincents Institute of Medical Research · AUWalter and Eliza Hall Institute of Medical Research · AUSt Vincent's Hospital · AUBarwon Health · AUInstitute for Medical Research · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effective osteoporosis therapy requires agents that increase the amount and/or quality of bone. Any modification of osteoclast-mediated bone resorption by disease or drug treatment, however, elicits a parallel change in osteoblast-mediated bone formation because the processes are tightly coupled. Anabolic approaches now focus on uncoupling osteoblast action from osteoclast formation, for example, by inhibiting sclerostin, an inhibitor of bone formation that does not influence osteoclast differentiation. Here, we report that oncostatin M (OSM) is produced by osteoblasts and osteocytes in mouse bone and that it has distinct effects when acting through 2 different receptors, OSM receptor (OSMR) and leukemia inhibitory factor receptor (LIFR). Specifically, mouse OSM (mOSM) inhibited sclerostin production in a stromal cell line and in primary murine osteoblast cultures by acting through LIFR. In contrast, when acting through OSMR, mOSM stimulated RANKL production and osteoclast formation. A key role for OSMR in bone turnover was confirmed by the osteopetrotic phenotype of mice lacking OSMR. Furthermore, in contrast to the accepted model, in which mOSM acts only through OSMR, mOSM inhibited sclerostin expression in Osmr-/- osteoblasts and enhanced bone formation in vivo. These data reveal what we believe to be a novel pathway by which bone formation can be stimulated independently of bone resorption and provide new insights into OSMR and LIFR signaling that are relevant to other medical conditions, including cardiovascular and neurodegenerative diseases and cancer.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBone and BonesBone DevelopmentBone Morphogenetic ProteinsBone ResorptionGenetic MarkersGlycoproteinsIntercellular Signaling Peptides and ProteinsLuciferasesMiceOncostatin MOrgan SizeOsteoblastsOsteocytesReceptors, Oncostatin MAdaptor Proteins, Signal TransducingBone Morphogenetic ProteinsGenetic MarkersGlycoproteinsIntercellular Signaling Peptides and ProteinsLuciferasesOncostatin MReceptors, Oncostatin MReceptors, OSM-LIFRNA, MessengerSost protein, mouse

Identifiers

PMID20051625
PMCPMC2810087
OpenAlexW2057035809

What OpenQuestion holds

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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.