ArticleJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry2009
Gadolinium-promoted cell cycle progression with enhanced S-phase entry via activation of both ERK and PI3K signaling pathways in NIH 3T3 cells.
Article in Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 26 citations in OpenAlex.
- Toxicity Mechanisms of Gadolinium and Gadolinium-Based Contrast Agents-A Review.International journal of molecular sciences · 2024Review
- Development and Characterization of Gadolinium and Copper Reinforced Bioactive Glass: An In Vitro Study.Cureus · 2024Article
- Benefits and Detriments of Gadolinium from Medical Advances to Health and Ecological Risks.Molecules (Basel, Switzerland) · 2020Review
- Gadolinium-doped bioglass scaffolds promote osteogenic differentiation of hBMSC via the Akt/GSK3β pathway and facilitate bone repair in vivo.International journal of nanomedicine · 2019Article
- Magnetic resonance functional nano-hydroxyapatite incorporated poly(caprolactone) composite scaffolds for in situ monitoring of bone tissue regeneration by MRI.Tissue engineering. Part A · 2014Article
- Integrin-mediated signaling contributes to gadolinium-containing-particle-promoted cell survival and G₁ to S phase cell cycle transition by enhancing focal adhesion formation.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2012Article
- Gadolinium-containing bioparticles as an active entity to promote cell cycle progression in mouse embryo fibroblast NIH3T3 cells.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
The aim of this study was to investigate whether Gd is able to exert the proliferation-promoting effect and to explore its possible underlying mechanism. We showed that Gd promoted cell cycle progression with increased S-phase entry in a concentration- and time-dependent manner in NIH 3T3 cells. The effect was further evidenced by the expressions of key proteins in driving cells through the G(1)/S transition point of the cell cycle. In the presence of Gd, the protein levels of cyclins D, E, and A were dramatically increased and demonstrated a characteristically temporal pattern of sequential mitotic events. Additionally, the levels of phosphorylated retinoblastoma protein were also significantly increased at certain time periods. To further elucidate the underlying mechanism, extracellular signal-regulated kinase and phosphatidylinositol 3-kinase signaling pathways were assessed. Both pathways were activated by Gd. Moreover, the levels of cyclin D and cyclin A were evaluated after the addition of the pharmacological inhibitors at early and late G(1) phases, correspondingly, to reveal the contribution of the two pathways in the Gd-promoted G(1)/S transition. It showed that both pathways were needed for Gd-promoted cell cycle progression. The results presented here provide novel evidence to advance knowledge leading to further understanding of the mechanisms of both cell growth and death caused by Gd and may be helpful for more rational application of Gd-based compounds in the future.
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