Evidence map›Paper›PMID 20348238›Full record

ArticleThe American journal of pathology2010

Immature osteoblast lineage cells increase osteoclastogenesis in osteogenesis imperfecta murine.

Haitao Li, Xi Jiang, John Delaney, Tiziana Franceschetti, Ines Bilic-Curcic, Judy Kalinovsky, Joseph A Lorenzo, Danka Grcevic, David W Rowe, Ivo Kalajzic

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  16. Review
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  18. Skeletal Response to Soluble Activin Receptor Type IIB in Mouse Models of Osteogenesis Imperfecta.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018
    Article
  19. Review
  20. Skeletal cell YAP and TAZ combinatorially promote bone development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
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

10 authors at 2 institutions in 2 countries.

Haitao LiDepartment of Reconstructive Sciences, University of Connecticut Health Center, Farmington, CT 06032, USA.
Xi Jiang
John Delaney
Tiziana Franceschetti
Ines Bilic-Curcic
Judy Kalinovsky
Joseph A Lorenzo
Danka Grcevic
David W Rowe
Ivo Kalajzic
UConn Health · USUniversity of Zagreb · HR

Funding

UConn Craniofacial Tissue Repair Regeneration ProgramU24DE016495 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI REISINE, SUSAN T · 2004 to 2005
$2.7M
Strategy to assess the function of osteocyte restricted genesR03AR053275 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI KALAJZIC, IVO · 2007 to 2009
$219k
NIAMS NIH HHS R03 AR053275NIAMS NIH HHS R03-AR053275NIDCR NIH HHS 5U24-DE016495-02NIDCR NIH HHS U24 DE016495
6 · The paper itself

Abstract

This study addressed the role of impairment of osteoblastic differentiation as a mechanism underlying pathophysiology of the osteogenesis imperfecta (OI). We hypothesized that combination of impaired osteogenic differentiation with increased bone resorption leads to diminished bone mass. By introducing visual markers of distinct stages of osteoblast differentiation, pOBCol3.6GFP (3.6GFP; preosteoblast) and pOBCol2.3GFP (2.3GFP; osteoblast/osteocytes), into the OIM model, we assessed osteoblast maturation and the mechanism of increased osteoclastogenesis. Cultures from oim/oim;2.3GFP mice showed a marked reduction of cells expressing GFP relative to +/+;2.3GFP littermates. No significant difference in expression of 3.6GFP between the +/+ and oim/oim mice was observed. Histological analysis of the oim/oim;3.6GFP mice showed an increased area of GFP-positive cells lining the endocortical surface compared with +/+;3.6GFP mice. In contrast GFP expression was similar between oim/oim;2.3GFP and +/+;2.3GFP mice. These data indicate that the osteoblastic lineage is under continuous stimulation; however, only a proportion of cells attain the mature osteoblast stage. Indeed, immature osteoblasts exhibit a stronger potential to support osteoclast formation and differentiation. We detected a higher Rankl/Opg ratio and higher expression of TNF-alpha in sorted immature osteoblasts. In addition, increased osteoclast formation was observed when osteoclast progenitors were cocultured with oim/oim-derived osteoblasts compared with osteoblasts derived from +/+ mice. Taken together, our data indicate that osteoblast lineage maturation is a critical aspect underlying the pathophysiology of OI.

Indexed as

AnimalsBone Marrow CellsCell LineageDisease Models, AnimalGreen Fluorescent ProteinsHomozygoteMiceMice, Inbred C3HMice, Inbred C57BLMice, TransgenicMutationOsteoblastsOsteoclastsOsteogenesis ImperfectaTumor Necrosis Factor-alphaGreen Fluorescent ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID20348238
PMCPMC2861105
OpenAlexW2120303417

What OpenQuestion holds

Textmetadata
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.