Hometown: Rootstown, OH
Education: BS from Mount Union University; Ph.D in Biomedical Science from Kent State University
Prostaglandins modulate an array of physiologic functions including insulin secretion and systemic inflammation. The EP3 and EP4 prostaglandin receptors play opposing roles in many cell types by signaling through different G proteins, resulting in inhibition (EP3) or 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 and pharmacological tools to examine the effects of EP3 and EP4 signaling in β-cell proliferation and survival in vivo and in ex vivo studies using rodent and human islets.