Dr. Hurley studies the genes responsible for maintaining healthy bones. She is also the Associate Dean of the Department of Health Career Opportunities Programs at UConn, which runs enrichment programs for middle school, high school, and college students to encourage those from underrepresented minorities to pursue a medical degree.

Dr. Hurley received her undergraduate and medical degrees from the University of Connecticut, completed a residency in internal medicine and a fellowship in endocrinology at the UConn Medical Center, and joined the faculty in 1986. She has received NIH funding for her research continuously since 1989. More recently, she received the Lawrence G. Raisz Award from the American Society for Bone and Mineral Research in 2016.

Osteoblasts (bone cells) produce FGF2, a growth factor found throughout the body that encourages cell proliferation and angiogenesis (blood vessel formation). Dr. Hurley’s lab is interested in understanding what FGF2 does in bone specifically, and how that knowledge can be harnessed to improve healing of broken bones and treatments for osteoporosis. Osteoporosis, a disease in which old bone is broken down faster than new bone is being produced, is estimated to impact 200 million people worldwide — particularly older women. Patients with osteoporosis are at much greater risk of bone fractures.

One facet of Dr. Hurley’s work has been to examine the interaction of FGF2 with another bone-related growth factor, BMP2. The body produces BMP2, which promotes new bone growth by inducing the precursor stem cells to differentiate into osteoblasts. It has been shown that applying synthesized BMP2 at the time of surgery can improve bone healing, and that combining it with FGF2 provides the same benefit from a lower dose of BMP2 (reducing side effects).

In a recent paper, Dr. Hurley and colleagues investigated a new way of delivering these two molecules to the site of a bone injury. Specifically, they wanted to know if FGF2 followed by BMP2 would be more effective for promoting healing than administration of the two simultaneously. They applied BMP2 to a commercially-available bone graft substitute, coated it with a barrier layer, and then applied the FGF2. The coating prevented the BMP2 underneath from being released for ~3 days, while the FGF2 was released immediately. The new graft resulted in better bone regeneration in mice with skull deformities than BMP2 on its own. This work is an exciting demonstration that delivering external growth factors sequentially (more similar to how it works internally) can be achieved with smart engineering of devices.