Russ Anthony

Throughout my entire career, my research has focused on pregnancy and pregnancy outcomes. This includes efforts focused on the establishment and maintenance of pregnancy, development of the placenta, placental function, and maternal/placental/fetal interactions in normal and compromised pregnancies. Over the years, our investigations have included protein purification and sequencing, examination of gene organization and sequence, specific gene transcriptional regulation, microarray and RNAseq assessment of gene expression, mRNA and protein expression, protein-protein interactions, maternal and fetal hormone concentrations, as well as in vivo assessment of altered placental function. While we have used various animal models, most of our research has used the pregnant sheep, not only because of its relevancy to livestock production, but also because the pregnant sheep has provided considerable insight into the physiology of pregnancy relevant to humans. This is in part due to the fact that we can chronically instrument/catheterize both the mother and fetus, allowing us to use the Fick Principle to determine steady-state uptake, transfer and utilization of oxygen, nutrients, hormones, etc., under non-stressed/non-anesthetized conditions (e.g., Regnault et al., 2003 and Barry et al., 2016). More recently we developed and validated lentiviral-mediated RNA interference (RNAi) approaches to alter placental gene expression in vivo (Purcell et al., 2009 and Baker et al., 2016). This approach allows the specific targeting of gene expression solely in placental trophoblast cells, and provides the mechanism to specifically study placental gene function in vivo in a variety of animal models, including the sheep. We have also expanded this approach to include the use of CRISPR-Cas9 constructs to allow direct gene-editing within the placenta in vivo. Currently we are funded by NIH to investigate the physiological ramifications of chorionic somatomammotropin (aka., placental lactogen) deficiency and to develop placental glucose transporter (SLC2A1 and SLC2A3) deficient pregnancies for in vivo study.