PSIII-1 Late-Breaking: Fighting Fetal Morbidity at the Fetal-Maternal Interface One Chemokine Access at a Time

Abstract Improper placentation is the root cause to intrauterine growth restriction (IUGR) and fetal mortality in livestock. This study aims further characterize importance of C-X-C motif chemokine receptor 4 (CXCR4) its ligand CXCL12 on through potential impacts insulin-like factors (IGF) their binding proteins (IGFBP1-3). CXCR4 are implicated though exact roles unclear. The peptides 1 2 have growth, placental development, trophoblast differentiation if IGFs down regulated, a corresponding decrease placenta fetus size has been observed. disease states like IUGR not completely known but studies demonstrated them be contributing factors. Using an in-vivo sheep model we surgically inserted osmotic pumps day 12 (d12) gestation ipsilateral corpus luteum deliver treatments into uterus bred ewes. Pumps delivered either saline (control) or AMD3100, inhibitor at 1x, 1.5x, 3x dose uterine lumen over course 14 days. Our objective was determine disrupting CXCL12/CXCR4 axis during implantation alters expression mid late gestation. At midgestation (d90) (d135) samples were obtained for analysis. Of targets tested, mRNA significantly decreased by AMD3100 treatment both IGF-1 (P = 0.05) IGF-2 0.02) compared control primarily maternal tissues d135. For tissue samples, d90 0.04) IGFBP-2 IGFBP-3 0.03) increased treated group while d135 IGF-1was 1x control. preliminary data show CXCL12- signaling that impairment this may alter multiple types later Insights will lead greater understanding development health mother offspring.