Presentation Type

Poster

Keywords

Semaphorin 7A, proliferation, migration, human umbilical vein endothelial cells, HUVEC

Department

Biology

Major

Biology

Abstract

Semaphorin 7A (SEMA 7A), a factor originally identified as regulating axon growth, has recently been implicated as a pro-angiogenic factor. The molecular mechanisms for this ability to stimulate angiogenesis have not been identified. This study examines if SEMA 7A can have a direct effect on vascular endothelial cells or whether it indirectly induces angiogenesis through stimulation and recruitment of macrophages as has been suggested. Using human umbilical vein endothelial cells (HUVECs), the ability of SEMA 7A to affect proliferation and migration was examined. HUVECs were exposed to SEMA 7A directly or to conditioned media collected from macrophages exposed to SEMA 7A and a cell proliferation assay was performed. Additionally, the ability of the cells to migrate was also measured using a transwell and a scratch assay. Direct exposure of HUVECs to SEMA 7A resulted in a significant decrease in cell proliferation. Preliminary results also suggest that direct exposure also results in a slight inhibitory effect on the migration of HUVECs. SEMA 7A treatment of macrophages did not result in the production of factors that stimulate HUVECs to proliferate. Additionally, our results suggest that macrophages exhibited a slight stimulation of migration in response to SEMA 7A.

Faculty Mentor

Donna Nofziger Plank

Funding Source or Research Program

Summer Undergraduate Research in Biology

Location

Waves Cafeteria, Tyler Campus Center

Start Date

21-3-2014 2:00 PM

End Date

21-3-2014 3:00 PM

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Mar 21st, 2:00 PM Mar 21st, 3:00 PM

The regulatory effect of semaphorin 7A on proliferation and migration in human umbilical vein endothelial cells

Waves Cafeteria, Tyler Campus Center

Semaphorin 7A (SEMA 7A), a factor originally identified as regulating axon growth, has recently been implicated as a pro-angiogenic factor. The molecular mechanisms for this ability to stimulate angiogenesis have not been identified. This study examines if SEMA 7A can have a direct effect on vascular endothelial cells or whether it indirectly induces angiogenesis through stimulation and recruitment of macrophages as has been suggested. Using human umbilical vein endothelial cells (HUVECs), the ability of SEMA 7A to affect proliferation and migration was examined. HUVECs were exposed to SEMA 7A directly or to conditioned media collected from macrophages exposed to SEMA 7A and a cell proliferation assay was performed. Additionally, the ability of the cells to migrate was also measured using a transwell and a scratch assay. Direct exposure of HUVECs to SEMA 7A resulted in a significant decrease in cell proliferation. Preliminary results also suggest that direct exposure also results in a slight inhibitory effect on the migration of HUVECs. SEMA 7A treatment of macrophages did not result in the production of factors that stimulate HUVECs to proliferate. Additionally, our results suggest that macrophages exhibited a slight stimulation of migration in response to SEMA 7A.