Evidence map›Paper›PMID 27253995›Full record

ArticleEndocrinology2016

Adult-Onset Deletion of β-Catenin in (10kb)Dmp1-Expressing Cells Prevents Intermittent PTH-Induced Bone Gain.

Rajendra Kedlaya, Kyung Shin Kang, Jung Min Hong, Vidya Bettagere, Kyung-Eun Lim, Daniel Horan, Paola Divieti-Pajevic, Alexander G Robling

Abstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Skeletal Effects of Inducible ERα Deletion in Osteocytes in Adult Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  6. Targeting the Wnt signaling pathway for breast cancer bone metastasis therapy.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  7. 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
  8. Article
  9. Article
  10. Expression of a Degradation-Resistant β-Catenin Mutant in Osteocytes Protects the Skeleton From Mechanodeprivation-Induced Bone Wasting.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  11. Article
  12. Article
  13. Regulation of Bone Remodeling by Parathyroid Hormone.Cold Spring Harbor perspectives in medicine · 2018
    Review
  14. Review
  15. 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

8 authors.

Rajendra KedlayaDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Kyung Shin KangDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Jung Min HongDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Vidya BettagereDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Kyung-Eun LimDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Daniel HoranDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Paola Divieti-PajevicDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.
Alexander G RoblingDepartment of Anatomy and Cell Biology (R.K., K.S.K., J.M.H., V.B., K.-E.L., D.H., A.G.R.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Department of Molecular and Cell Biology (P.D.-P.), Boston University School of Dental Medicine, Boston, Massachusetts 02215; Department of Biomedical Engineering (A.G.R.), Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202; and Richard L. Roudebush Veterans Affairs Medical Center (A.G.R.), Indianapolis, Indiana 46202.

Funding

Lrp5 signaling in bone mechanotransduction and metabolismR01AR053237 · NIAMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ALEXANDER G ROBLING, Matthew L Warman · 2005 to 2026
$9.4M
Improving bone health by harnessing the anabolic potential of LDL receptor relateI01BX001478 · VA · RLR VA MEDICAL CENTER · PI ROBLING, ALEXANDER G · 2012 to 2025
–
BLRD VA I01 BX001478NIAMS NIH HHS R01 AR053237
6 · The paper itself

Abstract

β-Catenin (βcat) is a major downstream signaling node in canonical Wingless-related integration site (Wnt) signaling pathway, and its activity is crucial for canonical Wnt signal transduction. Wnt signaling has recently been implicated in the osteo-anabolic response to PTH, a potent calcium-regulating factor. We investigated whether βcat is essential for the anabolic action of intermittent PTH by generating male mice with adult-onset deletion of βcat in a subpopulation of bone cells (osteocytes and late-stage osteoblasts), treating them with an anabolic regimen of PTH, and measuring the skeletal responses. Male (10kb)Dmp1-CreERt2 transgenic mice that also harbored floxed loss-of-function βcat alleles (βcat(f/f)) were induced for Cre activity using tamoxifen, then injected daily with human PTH 1-34 (30 μg/kg) or vehicle for 5 weeks. Mice in which βcat was deleted showed either total lack of bone mineral density (BMD) gain, or BMD loss, and did not respond to PTH treatment. However, bone mass measurements in the trabecular compartment of the femur and spine revealed PTH-induced bone gain whether βcat was deleted or not. PTH-stimulated increases in periosteal and cancellous bone formation rates were not impaired by βcat deletion, but resorption markers and cortical porosity were significantly increased in induced mice, particularly induced mice treated with PTH. These results suggest that βcat is required for net-positive BMD effects of PTH therapy but that the anabolic effects per se of PTH treatment might not require osteocytic/osteoblastic βcat.

Indexed as

Gene DeletionOsteogenesisAge FactorsAnabolic AgentsAnimalsbeta CateninBone DensityExtracellular Matrix ProteinsMaleMiceMice, Inbred C57BLMice, TransgenicMutagenesisParathyroid HormoneAnabolic Agentsbeta CateninDmp1 protein, mouseExtracellular Matrix ProteinsParathyroid Hormone

Identifiers

PMID27253995
PMCPMC4967118

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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.