David Olson (PhD, St. Louis University)
220 Heritage Medical Research Building
University of Alberta
Canada T6G 2S2
Tel: 780 492-2765
David Olson's website
Control of Birth / Control of Fetal Lung Development
Our laboratory is interested in perinatal physiology. The two areas we are actively exploring are the control of birth and lung development. In relation to birth, we are studying the regulation of prostaglandin (a ubiquitous fatty acid hormone) synthesis in human fetal membranes, decidua and placenta. Prostaglandins are considered essential in the initiation and maintenance of labor. We are examining the enzyme, prostaglandin endoperoxide H synthase (cyclooxygenase) from gene expression to enzyme activity. We know that PGHS-2 (inducible cyclooxygenase) is responsible for prostaglandins for birth. We use in vitro cell culture models of human intrauterine tissues to explore the effects of natural and pharmacological agonists on PGHS-2 activity and subsequent events leading to enhanced enzyme activity. As appropriate, we relate our in vitro studies to whole animal models in order to achieve a greater understanding of the control of birth. This is important, because a greater understanding of normal birth will lead to a better understanding of the causes of preterm birth.
Our studies in relation to lung development again center around the eicosanoids (prostaglandins and leukotrienes). We are actively exploring the role of eicosanoids in pulmonary cell growth, differentiation and maturation during the perinatal period. Other studies are exploring the regulation of prostaglandin and leukotriene synthesis during the perinatal period. For instance, we have recently learned that fetal and newborn breathing activity can influence the rate of prostaglandin synthesis. Again, we use whole animal, cell culture and biochemical approaches to answer the questions we are asking. A significant effort is directed towards understanding the role of eicosanoids in a disease of newborn (often times preterm, immature) infants known as pulmonary oxygen toxicity or bronchopulmonary dysplasia.
Whole animal experiments, pulmonary function measurements, cell culture, morphometric techniques, in situ hybridization, molecular biology.