Evidence map›Paper›PMID 26335301›Full record

ArticleJournal of endocrinological investigation2015

The endocrine disruptor cadmium alters human osteoblast-like Saos-2 cells homeostasis in vitro by alteration of Wnt/β-catenin pathway and activation of caspases.

V Papa, V M Bimonte, F Wannenes, A S D'Abusco, S Fittipaldi, R Scandurra, L Politi, C Crescioli, A Lenzi, L Di Luigi and 1 more

Abstract read
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In one paragraph

Article in Journal of endocrinological investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Airborne contaminant exposure and bone development: a systematic review and meta-analysis.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Pooled it
  2. Article
  3. Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Repercussions of Bisphenol A on the Physiology of Human Osteoblasts.International journal of molecular sciences · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Pleiotropic roles of CaToxicology letters · 2016
    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 2 institutions in 1 country.

V PapaDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy.
V M BimonteDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy.
F WannenesDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy.
A S D'AbuscoDepartment of Biochemistry, Section of Medical Pathophysiology, Endocrinology and Nutrition, "Sapienza" University of Rome, Rome, Italy.
S FittipaldiDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy.
R ScandurraDepartment of Biochemistry, Section of Medical Pathophysiology, Endocrinology and Nutrition, "Sapienza" University of Rome, Rome, Italy.
L PolitiDepartment of Biochemistry, Section of Medical Pathophysiology, Endocrinology and Nutrition, "Sapienza" University of Rome, Rome, Italy.
C CrescioliDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy.
A LenziDepartment of Experimental Medicine, Section of Medical Pathophysiology, Endocrinology and Nutrition, "Sapienza" University of Rome, Rome, Italy.
L Di LuigiDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy.
S MigliaccioDepartment of Movement, Human and Health Sciences, Section of Health Sciences, "Foro Italico" University of Rome, Largo Lauro De Bosis 15, 00195, Rome, Italy. silvia.migliaccio@uniroma4.it.
University of Catania · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe pollutant Cadmium (Cd) is widespread in the environment and causes alterations of human health by acting as an endocrine disruptor. Bone tissue seems to be a crucial target of Cd contamination. Indeed, we have previously demonstrated that this endocrine disruptor induces osteoblast apoptosis and necrosis. Thus, aim of this study was to further evaluate the effect of Cd on osteoblasts homeostasis, investigating potential modification of the Wnt/β-catenin intracellular pathway, the intracellular process involved in programmed cellular death and the cytoskeletal alterations. MATERIAL AND

methodsTo this purpose, human osteoblastic Saos-2 cells, a human osteosarcoma osteoblast-like cell line, were cultured and treated with Cd.

resultsOsteoblastic cells were treated for 6 h with 10μM Cd, which induced nuclear translocation of β-catenin and increased expression of Wnt/β-catenin target genes. Longer exposure to the same Cd concentration induced osteoblastic cell apoptosis. To better characterize the intracellular events involved in these Cd-induced alterations, we evaluated the effect of Cd exposure on actin filaments and proteins associated to cytoskeletal actin, characterized by the presence of LIM domains. Long (15, 24 h) exposure of osteoblasts to Cd reduced LIM proteins expression and induced actin filaments destruction and a significant caspase-3 activation after 24 h. In addition, to prove that Cd induces osteoblastic cells apoptosis after long exposure, we performed TUNEL assay which demonstrated increase of cell apoptosis after 24 h.

conclusionIn conclusion, our study shows that osteoblasts exposed to Cd for short intervals of time demonstrated an increase in cell proliferation through a Wnt/β-catenin dependent mechanism, likely as a compensatory mechanism in response to cell injury. Longer exposure to the same Cd concentration induced cells apoptosis through cytoskeleton disruption-mediated mechanisms and caspase activation.

Indexed as

Actin CytoskeletonApoptosisCadmiumCell DifferentiationCell Line, TumorEndocrine DisruptorsHomeostasisHumansIn Vitro TechniquesOsteoblastsWnt Signaling PathwayCadmiumEndocrine DisruptorsCadmiumDifferentiationOsteoblasts

Identifiers

PMID26335301
OpenAlexW1531427465

What OpenQuestion holds

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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.