Evidence map›Paper›PMID 27942992›Full record

ArticlePflugers Archiv : European journal of physiology2017

Increased bone resorption by osteoclast-specific deletion of the sodium/calcium exchanger isoform 1 (NCX1).

Giuseppe Albano, Silvia Dolder, Mark Siegrist, Annie Mercier-Zuber, Muriel Auberson, Candice Stoudmann, Willy Hofstetter, Olivier Bonny, Daniel G Fuster

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. The NaJournal of extracellular vesicles · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Membrane Transport Proteins in Osteoclasts: The Ins and Outs.Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. Increased levels of sodium chloride directly increase osteoclastic differentiation and resorption in mice and men.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017
    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

9 authors at 3 institutions in 1 country.

Giuseppe AlbanoDivision of Nephrology, Hypertension and Clinical Pharmacology, Bern University Hospital, University of Bern, Freiburgstrasse 15, 3010, Bern, Switzerland.
Silvia DolderNCCR Transcure, University of Bern, Bern, Switzerland.
Mark SiegristNCCR Transcure, University of Bern, Bern, Switzerland.
Annie Mercier-ZuberDepartment of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
Muriel AubersonDepartment of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
Candice StoudmannDepartment of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
Willy HofstetterNCCR Transcure, University of Bern, Bern, Switzerland.
Olivier BonnyDepartment of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
Daniel G FusterDivision of Nephrology, Hypertension and Clinical Pharmacology, Bern University Hospital, University of Bern, Freiburgstrasse 15, 3010, Bern, Switzerland. Daniel.Fuster@ibmm.unibe.ch.
University of Bern · CHUniversity of Lausanne · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium is a key component of the bone mineral hydroxyapatite. During osteoclast-mediated bone resorption, hydroxyapatite is dissolved and significant quantities of calcium are released. Several calcium transport systems have previously been identified in osteoclasts, including members of the sodium/calcium exchanger (NCX) family. Expression pattern and physiological role of NCX isoforms in osteoclasts, however, remain largely unknown at the moment. Our data indicate that all three NCX isoforms (NCX1, NCX2, and NCX3) are present in murine osteoclasts. RANKL-induced differentiation of murine osteoclast precursors into mature osteoclasts significantly attenuated the expression of NCX1, while NCX2 and NCX3 expressions were largely unaffected. To study the role of NCX1 during osteoclast differentiation and bone resorption, we crossed mice with exon 11 of the NCX1 gene flanked by loxP sites with cathepsin K-Cre transgenic mice. Mature osteoclasts derived from transgenic mice exhibited an 80-90% reduction of NCX1 protein. In vitro studies indicate that NCX1 is dispensable for osteoclast differentiation, but NCX1-deficient osteoclasts exhibited increased resorptive activity. In line with these in vitro findings, mice with an osteoclast-targeted deletion of the NCX1 gene locus displayed an age-dependent loss of bone mass. Thus, in summary, our data reveal NCX1 as a regulator of osteoclast-mediated bone resorption.

Indexed as

AnimalsBone ResorptionCalciumCell DifferentiationCell LineIon TransportMiceMice, Inbred C57BLMice, TransgenicOsteoclastsProtein IsoformsRANK LigandSequence DeletionSodiumSodium-Calcium ExchangerCalciumNCX1 protein, mouseProtein IsoformsRANK LigandSodiumSodium-Calcium ExchangerBoneNCX1OsteoclastSodium/calcium exchanger

Identifiers

PMID27942992
OpenAlexW2560029918

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.