Evidence map›Paper›PMID 23122304›Full record

ArticleCell calcium2012

Deletion of Orai1 alters expression of multiple genes during osteoclast and osteoblast maturation.

Sung-Yong Hwang, Julie Foley, Takuro Numaga-Tomita, John G Petranka, Gary S Bird, James W Putney

Abstract read
In one paragraph

Article in Cell calcium, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  3. Article
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  8. Role of KInternational journal of molecular sciences · 2021
    Review
  9. The function of the calcium channel Orai1 in osteoclast development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  10. ORAI1 CaFrontiers in cell and developmental biology · 2021
    Review
  11. Review
  12. Review
  13. Frontiers in physiology · 2020
    Review
  14. Calcium Signaling and Tissue Calcification.Cold Spring Harbor perspectives in biology · 2019
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

6 authors at 1 institution in 1 country.

Sung-Yong HwangLaboratory of Signal Transduction, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, NC 27709, USA.
Julie Foley
Takuro Numaga-Tomita
John G Petranka
Gary S Bird
James W Putney
National Institute of Environmental Health Sciences · US

Funding

Capacitative Calcium EntryZIAES090087 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRD, GARY · 2009 to 2019
$22.0M
Intramural NIH HHS ZIA ES090087
6 · The paper itself

Abstract

Store-operated Ca(2+) entry (SOCE) is a major Ca(2+) influx pathway in most non-excitable cell types and Orai1 was recently identified as an essential pore-subunit of SOCE channels. Here we investigate the physiological role of Orai1 in bone homeostasis using Orai1-deficient mice (Orai1(-/-)). Orai1(-/-) mice developed osteopenia with decreased bone mineral density and trabecular bone volume. To identify the nature and origin of the bone defect, bone-resorbing osteoclasts and bone-forming osteoblasts from Orai1(-/-) mice were examined. Orai1-mediated SOCE was completely abolished in Orai1(-/-) osteoclast precursor cells and osteoclastogenesis in vitro from Orai1(-/-) mice was impaired due to a defect in cell fusion of pre-osteoclasts. Also, resorption activity in vitro was comparable but the size of pits formed by Orai1(-/-) osteoclasts was smaller. We next assessed the role of Orai1 in osteoblast differentiation and function by using a pre-osteoblast cell line, as well as primary osteoblasts from wild-type and Orai1(-/-) mice. SOCE in MC3T3-E1 pre-osteoblastic cells was inactivated by lentiviral overexpression of a pore-dead Orai1 mutant. Lack of SOCE in MC3T3-E1 had no effect on alkaline phosphatase staining and expression but substantially inhibited mineralized nodule formation. Consistent with this finding, Orai1-mediated SOCE was markedly reduced in Orai1(-/-) osteoblast precursor cells and osteoblastogenesis in vitro from Orai1(-/-) stromal cells showed impaired mineral deposition but no change in differentiation. This indicates that Orai1 is involved in the function but not in the differentiation of osteoblasts. Together, these results suggest that Orai1 plays a critical role in bone homeostasis by regulating both osteoblasts and osteoclasts.

Indexed as

AnimalsCalciumCalcium ChannelsCell DifferentiationCell LineGene Expression RegulationMiceMice, Inbred C57BLMice, KnockoutORAI1 ProteinOsteoblastsOsteoclastsRANK LigandCalciumCalcium ChannelsORAI1 ProteinOrai1 protein, mouseRANK Ligand

Identifiers

PMID23122304
PMCPMC3511630
OpenAlexW2061207421

What OpenQuestion holds

Textmetadata
LicenceTDM
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.