Education
B.S n Biology from the University of Mount Union, Ph.D. from Kent State University Prostaglandins are important modulators of an array of physiologic functions including insulin secretion and systemic inflammation. EP3 and EP4 play opposing roles in many cell types due to signaling through different G proteins, resulting in Gi inhibition (EP3) or Gs stimulation (EP4) of adenylyl cyclase. We hypothesize that EP3 and EP4 play opposing roles in regulating β-cell mass expansion. Signaling via EP3 is predicted to inhibit β-cell proliferation whereas activation of EP4 is predicted to enhance β-cell proliferation and survival. I am using genetic
Prostaglandins (PGs) modulate an array of physiologic functions including insulin secretion and systemic inflammation. The PGE2 receptors, EP3 and EP4, play opposing roles in many cell types due to signaling through different G proteins, resulting in inhibition (EP3) or stimulation (EP4) of adenylyl cyclase. Signaling via EP3 is predicted to inhibit β-cell proliferation whereas activation of EP4 is predicted to enhance β-cell proliferation and survival. I am using genetic and pharmacological tools to examine the effect of EP3 and EP4 signaling in β-cell proliferation and survival in mouse models of diabetes and in rodent and human islets.