Event Title

Correlation Between Altered VEGF Signaling & Abnormal Skeletogenesis as a Result of Thalidomide Exposure in Developing Sea Urchin Embryos

Presenter Information

Alexis Aument
James Tsilionis

Faculty Advisor

Dr. Jan Reichard-Brown

Start Date

24-4-2018 5:00 PM

End Date

24-4-2018 6:00 PM

Description

During the 1950’s, thalidomide was a widely marketed drug given to pregnant women as a treatment for morning sickness. Its unforeseen teratogenicity resulted in over 10,000 children born with severe congenital birth defects. Thalidomide was withdrawn from the worldwide market in 1961. It returned to the U.S. market in 1997 due to its anti-angiogenic and anti-inflammatory properties under strict regulations and guidelines for its use. Today, thalidomide is used to effectively treat a variety of medical conditions and diseases. For over one-hundred years, sea urchin embryos have served as a model organism for early deuterostome development. Sea urchin embryos exposed to thalidomide in culture exhibit development delays, abnormal skeletogenesis and morphology. The vascular endothelial growth factor (VEGF) pathway is responsible for the migration of primary mesenchymal cells (PMCs) in sea urchins and angiogenesis in humans. Based upon studies in the literature, we hypothesize that thalidomide exposure following fertilization may disrupt the VEGF signaling pathway. Studies in this laboratory suggest that the PMCs of thalidomide treated embryos exhibit decreased VEGF staining compared to controls. In sea urchins, PMC migration is essential since the cells fuse to form the syncytial cables which serve as the axis for subsequent larval skeleton formation. Stored and fixed embryos treated with thalidomide will be examined using immune-histochemical staining with a labeled VEGF antibody. Alterations in VEGF signaling comparing thalidomide treated embryos to controls could indicate a potential correlation between thalidomide exposure and the disruption of the VEGF signaling pathway leading to abnormal skeletogenesis.

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Apr 24th, 5:00 PM Apr 24th, 6:00 PM

Correlation Between Altered VEGF Signaling & Abnormal Skeletogenesis as a Result of Thalidomide Exposure in Developing Sea Urchin Embryos

During the 1950’s, thalidomide was a widely marketed drug given to pregnant women as a treatment for morning sickness. Its unforeseen teratogenicity resulted in over 10,000 children born with severe congenital birth defects. Thalidomide was withdrawn from the worldwide market in 1961. It returned to the U.S. market in 1997 due to its anti-angiogenic and anti-inflammatory properties under strict regulations and guidelines for its use. Today, thalidomide is used to effectively treat a variety of medical conditions and diseases. For over one-hundred years, sea urchin embryos have served as a model organism for early deuterostome development. Sea urchin embryos exposed to thalidomide in culture exhibit development delays, abnormal skeletogenesis and morphology. The vascular endothelial growth factor (VEGF) pathway is responsible for the migration of primary mesenchymal cells (PMCs) in sea urchins and angiogenesis in humans. Based upon studies in the literature, we hypothesize that thalidomide exposure following fertilization may disrupt the VEGF signaling pathway. Studies in this laboratory suggest that the PMCs of thalidomide treated embryos exhibit decreased VEGF staining compared to controls. In sea urchins, PMC migration is essential since the cells fuse to form the syncytial cables which serve as the axis for subsequent larval skeleton formation. Stored and fixed embryos treated with thalidomide will be examined using immune-histochemical staining with a labeled VEGF antibody. Alterations in VEGF signaling comparing thalidomide treated embryos to controls could indicate a potential correlation between thalidomide exposure and the disruption of the VEGF signaling pathway leading to abnormal skeletogenesis.