Evidence map›Paper›PMID 20174869›Full record

ArticleTransgenic research2010

Human stanniocalcin-1 or -2 expressed in mice reduces bone size and severely inhibits cranial intramembranous bone growth.

Jennifer Johnston, Yudith Ramos-Valdes, Lee-Anne Stanton, Sadia Ladhani, Frank Beier, Gabriel E Dimattia

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Article in Transgenic research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  8. Article
  9. Expression, function and clinical application of stanniocalcin-1 in cancer.Journal of cellular and molecular medicine · 2020
    Review
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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.

Jennifer JohnstonCancer Research Laboratory Program, London Regional Cancer Program (LRCP), 790 Commissioners Rd, Room A4-921, London, ON, N6A 4L6, Canada.
Yudith Ramos-Valdes
Lee-Anne Stanton
Sadia Ladhani
Frank Beier
Gabriel E Dimattia
Western University · CA

Funding

Canadian Institutes of Health Research MOP 53128
6 · The paper itself

Abstract

Stanniocalcin-1 (STC1) and -2 (STC2) are highly related, secreted, homodimeric glycoproteins that are significantly upregulated by different forms of stress including high phosphate levels. Transgenic mice that constitutively express either human STC1 or STC2 exhibit intra-uterine growth restriction and permanent post-natal growth retardation. STC1 is expressed in chondrocytic and osteoblastic cells during murine development and can enhance differentiation of calvarial cells in culture. Therefore, there is mounting evidence that stanniocalcins (STCs) modulate bone development in vivo. To further define the effects of stanniocalcins on skeletal development, we performed a series of measurements on components of the axial, appendicular, and cranial skeleton in transgenic and wildtype mice. We show that skeletal growth is retarded and that the intramembranous bones of the cranium exhibit a particularly severe delay in suture closure. The posterior frontal suture remains patent throughout the lifetime of human STC1 and STC2 transgenic mice. We did not observe significant effects on chondrogenesis: however, calvarial cells exhibited reduced viability, proliferation and delayed differentiation, indicating that developing osteoblasts are particularly sensitive to the levels of STCs. Given the evidence linking STC1 to cellular phosphate homeostasis, we assessed the expression of a variety of phosphate regulators in transgenic and wildtype calvarial cells and found significantly lower levels of Mepe, Dmp1, Sfrp4 in transgenic cells without a change in Pit1 or Pit2. Collectively these data support a direct regulatory role for STCs in osteoblasts and suggest that overexposure to these factors inhibits normal skeletal development without significant changes in patterning.

Indexed as

AnimalsBase SequenceBone DevelopmentCranial SuturesDNA PrimersFemaleGene ExpressionGlycoproteinsGrowth PlateHumansIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicDNA PrimersGlycoproteinsIntercellular Signaling Peptides and ProteinsPhosphate Transport ProteinsRecombinant ProteinsSTC2 protein, humanteleocalcin

Identifiers

PMID20174869
OpenAlexW2150094179

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.