Evidence map›Paper›PMID 21412775›Full record

ArticleJournal of cellular physiology2012

Gremlin1 is required for skeletal development and postnatal skeletal homeostasis.

Ernesto Canalis, Kristen Parker, Stefano Zanotti

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  10. [The Mechanism of GREM1's Effect on Osteogenic/Odontogenic Differentiation of Stem Cells from Apical Papilla].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Article
  11. Article
  12. Article
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  14. Review
  15. Expression of Noggin and Gremlin1 and its implications in fine-tuning BMP activities in mouse cartilage tissues.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017
    Article
  16. Gremlin1 plays a key role in kidney development and renal fibrosis.American journal of physiology. Renal physiology · 2017
    Article
  17. Agonists and Antagonists of TGF-β Family Ligands.Cold Spring Harbor perspectives in biology · 2016
    Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Ernesto CanalisDepartment of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105-1299, USA. ecanalis@stfranciscare.org
Kristen Parker
Stefano Zanotti
Saint Francis Hospital & Medical Center · US

Funding

Growth Factors; Effect on Aspects of Bone FormationR01AR021707 · NIAMS · ST. FRANCIS HOSPITAL AND MEDICAL CENTER · PI CANALIS, ERNESTO · 1986 to 2012
$2.5M
GROWTH FACTORS EFFECT ON ASPECTS OF BONE FORMATIONR37AR021707 · NIAMS · ST. FRANCIS HOSPITAL AND MEDICAL CENTER · PI CANALIS, ERNESTO · 1992 to 2001
$624k
NIAMS NIH HHS AR021707NIAMS NIH HHS R01 AR021707NIAMS NIH HHS R37 AR021707
6 · The paper itself

Abstract

Gremlin is an antagonist of bone morphogenetic proteins, and its overexpression causes suppressed osteoblastogenesis and osteopenia. Inactivation of Grem1 results in severe developmental defects, but the consequences of the global inactivation of Grem1 on the postnatal skeleton are not known. To study the function of gremlin, Grem1 was inactivated by homologous recombination, and mice were maintained in a C57BL/6/FVB mixed genetic background due to embryonic and neonatal lethality in the uniform C57BL/6 background. Grem1 null mice exhibited developmental skeletal abnormalities, leading to incomplete formation of metatarsal bones and of fore limbs and hind limbs. Grem1 null mice exhibited decreased weight and body fat and shortened femoral length. Bone histomorphometric and microarchitectural analyses of distal femurs revealed decreased bone volume and increased bone formation in 1-month-old Grem1 null mice. Trabecular femoral bone volume was restored in older Grem1 null female mice, and to a lesser extent in male mice. Vertebral microarchitecture confirmed the osteopenia observed in 1-month-old Grem1 null mice and demonstrated recovery of trabecular bone in older female, but not in older male Grem1 null mice, which exhibited persistent vertebral osteopenia. In conclusion, Grem1 is not only necessary for skeletal development, but also for postnatal skeletal homeostasis; its inactivation causes osteopenia, which is partially reversed in a spatial, temporal, and sex-dependent manner due to an increase in bone formation.

Indexed as

AnimalsBone and BonesBone DensityBone Diseases, MetabolicCytokinesFemaleHomeostasisIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutOsteogenesisReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionCytokinesGrem1 protein, mouseIntercellular Signaling Peptides and Proteins

Identifiers

PMID21412775
PMCPMC3132213
OpenAlexW2106626619

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.