Evidence map›Paper›PMID 26481310›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

DMP-1-mediated Ghr gene recombination compromises skeletal development and impairs skeletal response to intermittent PTH.

Zhongbo Liu, Oran D Kennedy, Luis Cardoso, Jelena Basta-Pljakic, Nicola C Partridge, Mitchell B Schaffler, Clifford J Rosen, Shoshana Yakar

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Growth hormone receptor gene disruption.Vitamins and hormones · 2023
    Article
  7. Review
  8. Musculoskeletal Effects of Altered GH Action.Frontiers in physiology · 2022
    Review
  9. Article
  10. Anabolic actions of PTH in murine models: two decades of insights.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021
    Article
  11. Mouse models of growth hormone insensitivity.Reviews in endocrine & metabolic disorders · 2021
    Review
  12. Effects of GH/IGF axis on bone and cartilage.Molecular and cellular endocrinology · 2021
    Review
  13. Tissue-specific disruption of the growth hormone receptor (GHR) in mice: An update.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2020
    Review
  14. Review
  15. Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  16. Insulin-like growth factors: actions on the skeleton.Journal of molecular endocrinology · 2018
    Review
  17. Article
  18. Article
  19. Skeletal growth and bone mineral acquisition in type 1 diabetic children; abnormalities of the GH/IGF-1 axis.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2017
    Review
  20. 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

8 authors at 4 institutions in 1 country.

Zhongbo Liu*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Oran D Kennedy*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Luis Cardoso*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Jelena Basta-Pljakic*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Nicola C Partridge*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Mitchell B Schaffler*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Clifford J Rosen*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA.
Shoshana Yakar*Department of Basic Science and Craniofacial Biology, David B. Kriser Dental Center, New York University College of Dentistry, New York, New York, USA; Department of Biomedical Engineering, City College of New York, New York, New York, USA; and Maine Medical Center Research Institute, Scarborough, Maine, USA sy1007@nyu.edu.
New York University · USNew York University Langone Orthopedic Hospital · USCity College of New York · USMaine Medical Center Research Institute · US

Funding

Nuclear Events in PTHR1 Action on BoneR01DK047420 · NIDDK · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Nicola C Partridge · 1994 to 2026
$8.0M
Osteocyte Integrity and Bone RemodelingR01AR041210 · NIAMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SCHAFFLER, MITCHELL B · 1997 to 2019
$5.8M
Progenitor Cell Analysis CoreP30GM106391 · NIGMS · MAINEHEALTH · PI FRIESEL, ROBERT E · 2013 to 2017
$5.7M
Structural, Molecular, and Functional Specialization in Osteocyte MechanosensingR01AR057139 · NIAMS · CITY COLLEGE OF NEW YORK · PI SCHAFFLER, MITCHELL B, SPRAY, DAVID C · 2010 to 2014
$2.5M
Central Role for Osteocytes in Integration of Endocrine Signals During GrowthR01DK100246 · NIDDK · NEW YORK UNIVERSITY · PI YAKAR, SHOSHANA · 2014 to 2017
$1.3M
MICRODAMAGE AND BONE REMODELING IN STRESS FRACTURER29AR041210 · NIAMS · HENRY FORD HEALTH SYSTEM · PI SCHAFFLER, MITCHELL B · 1992 to 1996
–
NIAMS NIH HHS AR041210NIAMS NIH HHS AR057139NIAMS NIH HHS R01 AR041210NIAMS NIH HHS R01 AR057139NIDDK NIH HHS DK100246NIDDK NIH HHS R01 DK047420NIDDK NIH HHS R01 DK100246NIGMS NIH HHS P30 GM106391
6 · The paper itself

Abstract

Bone minerals are acquired during growth and are key determinants of adult skeletal health. During puberty, the serum levels of growth hormone (GH) and its downstream effector IGF-1 increase and play critical roles in bone acquisition. The goal of the current study was to determine how bone cells integrate signals from the GH/IGF-1 to enhance skeletal mineralization and strength during pubertal growth. Osteocytes, the most abundant bone cells, were shown to orchestrate bone modeling during growth. We used dentin matrix protein (Dmp)-1-mediated Ghr knockout (DMP-GHRKO) mice to address the role of the GH/IGF axis in osteocytes. We found that DMP-GHRKO did not affect linear growth but compromised overall bone accrual. DMP-GHRKO mice exhibited reduced serum inorganic phosphate and parathyroid hormone (PTH) levels and decreased bone formation indices and were associated with an impaired response to intermittent PTH treatment. Using an osteocyte-like cell line along with in vivo studies, we found that PTH sensitized the response of bone to GH by increasing Janus kinase-2 and IGF-1R protein levels. We concluded that endogenously secreted PTH and GHR signaling in bone are necessary to establish radial bone growth and optimize mineral acquisition during growth.

Indexed as

AnimalsBone DensityBone DevelopmentCarrier ProteinsCell LineExtracellular Matrix ProteinsFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGene Expression RegulationMaleMiceMice, Inbred C57BLMice, KnockoutParathyroid HormonePhosphorusCarrier ProteinsDmp1 protein, mouseExtracellular Matrix ProteinsFibroblast Growth Factor-23Fibroblast Growth FactorsParathyroid HormonePhosphorussomatotropin-binding proteinfibroblast growth factor-23growth hormone receptormicrocomputed tomographyosteocyteparathyroid hormone

Identifiers

PMID26481310
PMCPMC4714547
OpenAlexW1816275380

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.