Evidence map›Paper›PMID 26276370›Full record

ArticleJournal of dental research2015

PTH and Vitamin D Repress DMP1 in Cementoblasts.

L Wang, A B Tran, F H Nociti, V Thumbigere-Math, B L Foster, C C Krieger, K R Kantovitz, C M Novince, A J Koh, L K McCauley and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of dental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Mechanisms of phosphate transport.Nature reviews. Nephrology · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. 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

11 authors at 5 institutions in 2 countries.

L WangNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA le.wang@nih.gov.
A B TranNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA.
F H NocitiNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry, Campinas State University, Piracicaba, SP, Brazil.
V Thumbigere-MathNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA.
B L FosterNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA.
C C KriegerNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, MD, USA.
K R KantovitzNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry, Campinas State University, Piracicaba, SP, Brazil.
C M NovinceSchool of Dentistry, University of Michigan, Ann Arbor, MI, USA Department of Oral Health Sciences, Medical University of South Carolina, Charleston, SC, USA.
A J KohSchool of Dentistry, University of Michigan, Ann Arbor, MI, USA.
L K McCauleySchool of Dentistry, University of Michigan, Ann Arbor, MI, USA.
M J SomermanNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA.
National Institutes of Health · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · USUniversity of Michigan–Ann Arbor · USMedical University of South Carolina · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

NIAMS Light Imaging FacilityZICAR041186 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RANDAZZO, DAVIDE · 2010 to 2025
$18.2M
Laboratory of Oral Connective Tissue BiologyZIAAR041196 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SOMERMAN, MARTHA · 2013 to 2021
$8.9M
ANABOLIC MECHANISMS OF PTH ACTION IN BONER01DK053904 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MCCAULEY, LAURIE K. · 1998 to 2016
$4.6M
Extracellular Matrix and Phosphate/Pyrophosphate Metabolism in Cementum FormationR00AR066110 · NIAMS · OHIO STATE UNIVERSITY · PI FOSTER, BRIAN LEE · 2015 to 2017
$747k
Intramural NIH HHSNIAMS NIH HHS R00 AR066110NIDDK NIH HHS R01 DK053904NIDDK NIH HHS R01DK53904
6 · The paper itself

Abstract

A complex feedback mechanism between parathyroid hormone (PTH), 1,25(OH)2D3 (1,25D), and fibroblast growth factor 23 (FGF-23) maintains mineral homeostasis, in part by regulating calcium and phosphate absorption/reabsorption. Previously, we showed that 1,25D regulates mineral homeostasis by repressing dentin matrix protein 1 (DMP1) via the vitamin D receptor pathway. Similar to 1,25D, PTH may modulate DMP1, but the underlying mechanism remains unknown. Immortalized murine cementoblasts (OCCM.30), similar to osteoblasts and known to express DMP1, were treated with PTH (1-34). Real-time quantitative polymerase chain reaction (PCR) and Western blot revealed that PTH decreased DMP1 gene transcription (85%) and protein expression (30%), respectively. PTH mediated the downregulation of DMP1 via the cAMP/protein kinase A (PKA) pathway. Immunohistochemistry confirmed the decreased localization of DMP1 in vivo in cellular cementum and alveolar bone of mice treated with a single dose (50 µg/kg) of PTH (1-34). RNA-seq was employed to further identify patterns of gene expression shared by PTH and 1,25D in regulating DMP1, as well as other factors involved in mineral homeostasis. PTH and 1,25D mutually upregulated 36 genes and mutually downregulated 27 genes by ≥2-fold expression (P ≤ 0.05). Many identified genes were linked with the regulation of bone/tooth homeostasis, cell growth and differentiation, calcium signaling, and DMP1 transcription. Validation of RNA-seq results via PCR array confirmed a similar gene expression pattern in response to PTH and 1,25D treatment. Collectively, these results suggest that PTH and 1,25D share complementary effects in maintaining mineral homeostasis by mutual regulation of genes/proteins associated with calcium and phosphate metabolism while also exerting distinct roles on factors modulating mineral metabolism. Furthermore, PTH may modulate phosphate homeostasis by downregulating DMP1 expression via the cAMP/PKA pathway. Targeting genes/proteins mutually governed by PTH and 1,25D may be a viable approach for designing new therapies for preserving mineralized tissue health.

Indexed as

AnimalsBlotting, WesternCell LineCyclic AMP-Dependent Protein KinasesDental CementumDown-RegulationExtracellular Matrix ProteinsFibroblast Growth Factor-23Fluorescent Antibody TechniqueGene ExpressionMiceParathyroid HormoneReal-Time Polymerase Chain ReactionVitamin DCyclic AMP-Dependent Protein KinasesDmp1 protein, mouseExtracellular Matrix ProteinsFgf23 protein, mouseFibroblast Growth Factor-23Parathyroid HormoneVitamin D1,25Ddentin matrix protein 1hormonal regulationmineral homeostasisparathyroid hormoneRNA sequencing

Identifiers

PMID26276370
PMCPMC4577985
OpenAlexW1539685921

What OpenQuestion holds

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Registered trials

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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.