Evidence map›Paper›PMID 25538250›Full record

ArticleThe Journal of biological chemistry2015

Osteoblast menin regulates bone mass in vivo.

Ippei Kanazawa, Lucie Canaff, Jad Abi Rafeh, Aarti Angrula, Jingjing Li, Ryan C Riddle, Iris Boraschi-Diaz, Svetlana V Komarova, Thomas L Clemens, Monzur Murshed and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  8. Review
  9. The role of menin in bone pathology.Endocrine connections · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
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  19. Multiple Endocrine Neoplasia: Genetics and Clinical Management.Surgical oncology clinics of North America · 2015
    Review
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

11 authors at 5 institutions in 3 countries.

Ippei KanazawaFrom the Departments of Medicine.
Lucie CanaffFrom the Departments of Medicine.
Jad Abi RafehPhysiology.
Aarti AngrulaFrom the Departments of Medicine.
Jingjing LiDentistry.
Ryan C RiddleDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and the Veterans Administration Medical Center, Baltimore, Maryland 21201.
Iris Boraschi-DiazDentistry.
Svetlana V KomarovaDentistry.
Thomas L ClemensDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and the Veterans Administration Medical Center, Baltimore, Maryland 21201.
Monzur MurshedFrom the Departments of Medicine, Dentistry.
Geoffrey N HendyFrom the Departments of Medicine, Physiology, Human Genetics, and Calcium Research Laboratory, and Hormones and Cancer Research Unit, Royal Victoria Hospital, McGill University, Montreal, Quebec H3A 1A1, Canada, geoffrey.hendy@mcgill.ca.
Royal Victoria Hospital · CAMcGill University · CAJohns Hopkins Medicine · USUnited States Department of Veterans Affairs · USUniversity of Dental Medicine · MM

Funding

Canadian Institutes of Health Research 123310Canadian Institutes of Health Research 776403Canadian Institutes of Health Research MOP-9315
6 · The paper itself

Abstract

Menin, the product of the multiple endocrine neoplasia type 1 (Men1) tumor suppressor gene, mediates the cell proliferation and differentiation actions of transforming growth factor-β (TGF-β) ligand family members. In vitro, menin modulates osteoblastogenesis and osteoblast differentiation promoted and sustained by bone morphogenetic protein-2 (BMP-2) and TGF-β, respectively. To examine the in vivo function of menin in bone, we conditionally inactivated Men1 in mature osteoblasts by crossing osteocalcin (OC)-Cre mice with floxed Men1 (Men1(f/f)) mice to generate mice lacking menin in differentiating osteoblasts (OC-Cre;Men1(f/f) mice). These mice displayed significant reduction in bone mineral density, trabecular bone volume, and cortical bone thickness compared with control littermates. Osteoblast and osteoclast number as well as mineral apposition rate were significantly reduced, whereas osteocyte number was increased. Primary calvarial osteoblasts proliferated more quickly but had deficient mineral apposition and alkaline phosphatase activity. Although the mRNA expression of osteoblast marker and cyclin-dependent kinase inhibitor genes were all reduced, that of cyclin-dependent kinase, osteocyte marker, and pro-apoptotic genes were increased in isolated Men1 knock-out osteoblasts compared with controls. In contrast to the knock-out mice, transgenic mice overexpressing a human menin cDNA in osteoblasts driven by the 2.3-kb Col1a1 promoter, showed a gain of bone mass relative to control littermates. Osteoblast number and mineral apposition rate were significantly increased in the Col1a1-Menin-Tg mice. Therefore, osteoblast menin plays a key role in bone development, remodeling, and maintenance.

Indexed as

Cell DifferentiationAnimalsApoptosisBlotting, WesternBone and BonesBone DensityBone DevelopmentBone Morphogenetic Protein 2Cell ProliferationCells, CulturedFemaleHumansMaleMiceMice, KnockoutMice, TransgenicBone Morphogenetic Protein 2MEN1 protein, humanMen1 protein, mouseProto-Oncogene ProteinsRNA, MessengerTransforming Growth Factor betaBoneBone Morphogenetic Protein (BMP)Gene KnockoutMeninMouseOsteoblastOsteoclastOsteocyteTransforming Growth Factor β (TGF-B)

Identifiers

PMID25538250
PMCPMC4326801
OpenAlexW1986214518

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.