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Gadolinium promoted proliferation in mouse embryo fibroblast NIH3T3 cells through Rac and PI3K/Akt signaling pathways

Biometals, 2014-08, Vol.27 (4), p.753-762 [Peer Reviewed Journal]

Springer Science+Business Media New York 2014 ;ISSN: 0966-0844 ;EISSN: 1572-8773 ;DOI: 10.1007/s10534-014-9769-9 ;PMID: 25037060

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Title:
Gadolinium promoted proliferation in mouse embryo fibroblast NIH3T3 cells through Rac and PI3K/Akt signaling pathways
Author: Shen, Liming ; Yang, Aochu ; Yao, Pengwei ; Sun, Xiaohong ; Chen, Cheng ; Mo, Cuiping ; Shi, Lei ; Chen, Youjiao ; Liu, Qiong
Subjects: Aminoquinolines - pharmacology ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell growth ; Cell Movement ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Contrast Media - toxicity ; Cytoskeleton - drug effects ; Cytoskeleton - metabolism ; Embryos ; Exposure ; Fibroblasts ; Fibrosis ; Gadolinium ; Gadolinium - toxicity ; Inhibitors ; Life Sciences ; Medicine/Public Health ; Metals ; Mice ; Microbiology ; Migration ; Neuropeptides - antagonists & inhibitors ; Neuropeptides - metabolism ; NIH 3T3 Cells ; Pathogenesis ; Pathways ; Pharmacology/Toxicology ; Phosphatidylinositol 3-Kinases ; Phosphorylation ; Plant Physiology ; Protein Processing, Post-Translational ; Proto-Oncogene Proteins c-akt - metabolism ; Pyrimidines - pharmacology ; rac1 GTP-Binding Protein - antagonists & inhibitors ; rac1 GTP-Binding Protein - metabolism ; Reactive Oxygen Species - metabolism ; Rodents ; Signal Transduction ; Survival
Is Part Of: Biometals, 2014-08, Vol.27 (4), p.753-762
Description: Nephrogenic systemic fibrosis (NSF) is a fibrosing disorder disease developed in patients with underlying renal insufficiency following exposure to gadolinium-based contrast agents (GBCAs). Previous studies have demonstrated that GdCl 3 can promote NIH3T3 fibroblast cell proliferation, which provide a new clue to the role of GBCAs in the development of NSF. In the present study, we further clarify the molecular mechanism of Gd-promoted proliferation. The results showed that intervention with the Rac inhibitor NSC23766 abrogated Gd-promoted proliferation. The levels of active Rac1 significantly increased in Gd-treated cells detected by pull-down assays. In addition, the phosphorylation of Akt was significantly elevated in the treatment group, which was blocked by NSC23766. NSC23766 also reduced the migration of NIH3T3 cells enhanced by Gd. Moreover, the F-actin cytoskeleton was strengthened and the mitotic cell numbers was significantly increased after exposure to Gd. These results suggest that Rac and PI3K/Akt signaling pathways, as well as integrin-mediated signal pathway may play important roles in Gd-induced cell proliferation. In addition, under serum-free condition, Gd could decrease ROS accumulation and increase NIH3T3 cell survival.
Publisher: Dordrecht: Springer Netherlands
Language: English;Dutch
Identifier: ISSN: 0966-0844
EISSN: 1572-8773
DOI: 10.1007/s10534-014-9769-9
PMID: 25037060
Source: MEDLINE
Alma/SFX Local Collection
ProQuest Central

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Gadolinium promoted proliferation in mouse embryo fibroblast NIH3T3 cells through Rac and PI3K/Akt signaling pathways

Springer Science+Business Media New York 2014 ;ISSN: 0966-0844 ;EISSN: 1572-8773 ;DOI: 10.1007/s10534-014-9769-9 ;PMID: 25037060

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