Obesity is a global threat. Previous studies determined that maternal obesity increases the likelihood of obese offspring with lifelong complications. Specifically, prior to implantation, the early embryonic period is susceptible to the effects of obesity, which causes proinflammatory adipokines to promote white adipose tissue (WAT) dysfunction. Through oxidative stress in WAT, it is proposed that ruptured-mitochondria release mitochondrial DNA (mtDNA) that is harbored in extracellular vesicles (EVs). Being crucial communication molecules, EVs carry cargo such as mitochondria or mtDNA to distal sites that can induce inflammation and activate an immune response. Thus, the Simmons Lab hypothesizes that maternal obesity causes WAT to release EVs that contain mtDNA or mitochondria that then migrate to the preimplantation embryo and induce abnormal metabolic function of the offspring. 

In order to follow mitochondrial migration in EVs from maternal adipose tissue, our group is crossing several  transgenic murine lines  with the goal of producing a mouse that has red fluorescent mitochondria in green fluorescent-tagged EVs from adipocytes. This model will enable us to track  adipocyte EVs in vivo and in vitrovia fluorescent microscopy, compare the concentration/content of EVs, determine the functional effects of EVs, determine viability of embryos exposed to EVs from obese dams, and determine if EVs are transported to the inner cell mass or the trophectoderm of the embryo. To perform colony maintenance, I had the responsibility of determining the zygosity of the transgenic mice this summer. Under the guidance of Lindsey Block and the leadership of Dr. Simmons at the Center for Research on Reproduction and Women’s Health at Perelman Medicine, I am grateful to have been provided a worthwhile introduction to reproductive health research at Penn.