Inducing Maternal Hyperthyroidism in Chicken Embryos to Study Involvement in FGFR1 Pathway

Hannah M. Ankrom*, Carson L. Corrick*, Holly L. Racine
West Liberty University, Department of Biology, West Liberty, WV 26074

Presentation Category: Biological Sciences (Poster Presentation)

Student’s Major: Pre-Medicine

Craniosynostosis (CS) is the premature fusion of the cranial sutures. CS causes increased cranial pressure and skull deformities. Maternal hyperthyroidism is linked to the development of CS in utero, but the exact mechanism is unknown. One proposed mechanism is increased action of thyroid hormone (TH) on the fibroblast growth factor receptor 1 (FGFR1). To understand this pathway, we used an avian model to mimic maternal hyperthyroidism. Our hypothesis is that injection of TH into the fertilized chicken egg will increase expression of FGFR1 in cranial tissue. We injected chicken eggs (N=21) with saline (N=11) and TH (N=10) every other day from E4 to E18 and harvested on E19. We discovered that 100% of our TH-injected eggs did not survive the injections. However, viability of embryos injected with saline was 90%. It is suspected the embryos were not able to compensate for the excess TH since the thyroid gland does not develop until E10. Current studies are focused on developing a more efficient dosing regimen. Existing saline-injected eggs serve as controls for examining FGFR1 expression.

Funding: NASA West Virginia Space Grant Consortium, Grant # 80NSSC20M0055

Program/mechanism supporting research/creative efforts: a West Virginia SURE program