MAPKs and PI3K/Akt pathways are involved in G-CSF-induced migration in a human trophoblast cell line

FURMENTO V.A.; BLANK VC; MADHIVANAN K; AGUILAR C; MARINO V.J.; ROGUIN, L. P

Mar del Plata

Simposio; 6th Latin American Symposium on Maternal-Fetal Interaction and Placenta. 5th Latin American Symposium on Reproductive Immunology; 2015

CONICET, INNOVA-T, IFPA, PAA

The relevance of the hematopoietic cytokine Granulocyte-Colony Stimulating Factor (G-CSF) signaling and the biological function of G-CSF:G-CSF receptor interaction in placental tissue has been the focus of our lab for the last years. In this sense, we have previously reported that G-CSF upregulates MMP-2 and VEGF through PI3K/Akt and Erk1/2 activation in the human first trimester trophoblast Swan 71 cell line. Objectives: The aim of our work was to examine whether G-CSF modifies β1-integrin expression levels and actin cytoskeleton organization in Swan 71 cells. In addition, we studied the effect of G-CSF on cell migration as well as the signaling pathways involved in this process. Methods: G-CSF effect on Swan 71 actin cytoskeleton was explored by immunocytochemistry after rodamin-phalloidin staining. β1-integrin expression levels following G-CSF stimulation were determined by Western blot assays. Cell migration was assessed by transwell chambers (Tr) and wound healing (Wh) assays. Pharmacological inhibitors and dominant negative mutants (DN) were used in Wh migration assays to inhibit MAPKs and PI3K/Akt pathways. Results: G-CSF induced actin cytoskeleton rearrangement (migratory phenotype) after 9 hr of stimulation (p