Journal
EXPERIMENTAL CELL RESEARCH
Volume 342, Issue 2, Pages 125-134Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2016.03.005
Keywords
G-CSF; Swan 71 cells; MAPK; PI3K; Migration; beta 1 Integrin
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Funding
- Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET) [PIP 0066]
- Agencia Nacional de Promocion Cientifica y Tecnologica [PICT-2012-1328]
- Universidad de Buenos Aires [UBACYT 20020130100024, 20020130100289]
- National Institute of Health [5 R21 CA151961]
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Multiple cytokines and growth factors expressed at the fetal-maternal interface are involved in the regulation of trophoblast functions and placental growth, but the role of G-CSF has not been completely established. Based on our previous study showing that G-CSF increases the activity of matrix metallo-proteinase-2 and the release of vascular endothelial growth factor in Swan 71 human trophoblast cells, in this work we explore the possible contribution of G-CSF to cell migration and the G-CSF-triggered signaling pathway. We found that G-CSF induced morphological changes on actin cytoskeleton consistent with a migratory cell phenotype. G-CSF also up-regulated the expression levels of beta 1 integrin and promoted Swan 71 cell migration. By using selective pharmacological inhibitors and dominant negative mutants we showed that PI3K, Erk 1/2 and p38 pathways are required for promoting Swan 71 cell motility. It was also demonstrated that PI3K behaved as an upstream regulator of Erk 1/2 and p38 MAPK. In addition, the increase of beta 1 integrin expression was dependent on PI3K activation. In conclusion, our results indicate that G-CSF stimulates beta 1 integrin expression and Swan 71 cell migration by activating PI3K and MAPK signaling pathways, suggesting that G-CSF should be considered as an additional regulatory factor that contributes to a successful embryo implantation and to the placenta development. (C) 2016 Elsevier Inc. All rights reserved.
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