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Announcement of DTM Pilot Studies Grants

“Novel Role for EGLN3 in Mediating Tolerance to Hypoxia at Birth”

Robert S. Freeman, Ph.D., Department of Pharmacology and Physiology
Michael A. O’Reilly, Ph.D., Department of Pediatrics

Robert Freeman, Ph.D.

Robert S. Freeman, Ph.D.

Michael A. O'Reilly, Ph.D.

Michael A. O’Reilly, Ph.D.

Birth is often complicated by events that reduce or disrupt oxygen delivery to critical tissues in the fetus and newborn, which if severe or sustained, can lead to cerebral palsy, intellectual and behavioral disabilities, or death. Fortunately, in most instances the resulting hypoxia is moderate or transient and is well tolerated due to a variety of incompletely understood adaptations that maximize O2 extraction while minimizing O2 consumption. Using a mouse model of perinatal hypoxia, we are testing the hypothesis that the EGLN3 gene, which encodes an oxygen-sensing prolyl hydroxylase, is an important mediator of the compensatory mechanisms that allow the term fetus and newborn to tolerate hypoxia at birth.

“Fibronectin-Driven Mechanisms of Embryonic Tendon Development”

Denise C. Hocking, Ph.D. – Department of Pharmacology and Physiology
Catherine K. Kuo, Ph.D. – Department of Biomedical Engineering

Denise Hocking, Ph.D.

Denise C. Hocking, Ph.D.

Catherine Kuo, Ph.D.

Catherine K. Kuo, Ph.D.

Tendons convert skeletal muscle contraction into joint movement. In the U.S., ~15 million tendon injuries occur each year requiring treatment costs that exceed US$30 billon. Injured tendons heal as dysfunctional scar tissue when partially ruptured, and do not heal at all when fully ruptured. In contrast to adult tendons, tendon healing in the fetus proceeds normally without scar formation. The goal of this project is to examine extracellular matrix (ECM) fibronectin-driven mechanisms of tendon development, and to use this information as a tissue engineering strategy for tendon replacement therapies.