ArticleFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association2012
Cadmium exposure activates the ERK signaling pathway leading to altered osteoblast gene expression and apoptotic death in Saos-2 cells.
Article in Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Urine Cadmium as a Risk Factor for Osteoporosis and Osteopenia: A Meta-Analysis.Frontiers in medicine · 2021Pooled it
- Mechanisms of Phytoremediation by Resveratrol against Cadmium Toxicity.Antioxidants (Basel, Switzerland) · 2024Review
- Prolonged Cadmium Exposure and Osteoclastogenesis: A Mechanistic Mouse andEnvironmental health perspectives · 2024Article
- Cadmium-induced annulus fibrosus cell senescence contributes to intervertebral disc degeneration via the JNK/p53 signaling pathway.Iranian journal of basic medical sciences · 2024Article
- ERK: A Double-Edged Sword in Cancer. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer.Cells · 2021Review
- Mechanical strain-mediated reduction in RANKL expression is associated with RUNX2 and BRD2.Gene: X · 2020Article
- The Role of Natural Antioxidants Against Reactive Oxygen Species Produced by Cadmium Toxicity: A Review.Advanced pharmaceutical bulletin · 2020Review
- Electronic cigarette liquid exposure induces flavor-dependent osteotoxicity and increases expression of a key bone marker, collagen type I.Journal of applied toxicology : JAT · 2019Article
- Article
- Pleiotropic roles of CaToxicology letters · 2016Article
- Role of autophagy in cadmium-induced apoptosis of primary rat osteoblasts.Scientific reports · 2016Article
- Cadmium induces apoptosis in primary rat osteoblasts through caspase and mitogen-activated protein kinase pathways.Journal of veterinary science · 2015Article
- Changes in compact bone microstructure of rats subchronically exposed to cadmium.Acta veterinaria Scandinavica · 2014Article
- Environmental cadmium exposure and osteoporosis: a review.International journal of public health · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recent reports of cadmium in electronic waste and jewelry have increased public awareness regarding this toxic metal. Human exposure to cadmium is associated with the development of osteoporosis. We previously reported cadmium induces apoptosis in human tumor-derived Saos-2 osteoblasts. In this study, we examine the extracellular signal-regulated protein kinase (ERK) and protein kinase C (PKC) pathways in cadmium-induced apoptosis and altered osteoblast gene expression. Saos-2 osteoblasts were cultured in the presence or absence of 10μM CdCl(2) for 2-72h. We detected significant ERK activation in response to CdCl(2) and pretreatment with the ERK inhibitor PD98059 attenuated cadmium-induced apoptosis. However, PKCα activation was not observed after exposure to CdCl(2) and pretreatment with the PKC inhibitor, Calphostin C, was unable to rescue cells from cadmium-induced apoptosis. Gene expression studies were conducted using qPCR. Cells exposed to CdCl(2) exhibited a significant decrease in the bone-forming genes osteopontin (OPN) and alkaline phosphatase (ALP) mRNA. In contrast, SOST, whose protein product inhibits bone formation, significantly increased in response to CdCl(2). Pretreatment with PD98059 had a recovery effect on cadmium-induced changes in gene expression. This research demonstrates cadmium can directly inhibit osteoblasts via ERK signaling pathway and identifies SOST as a target for cadmium-induced osteotoxicity.
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Registered trials
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.