Presentation Title

Nonsteroidal Anti-inflammatory Drug Effects on Angiogenic Responses in HUVECs

Start Date

November 2016

End Date

November 2016

Location

HUB 302-70

Type of Presentation

Poster

Abstract

Angiogenesis is the process through which new blood vessels form in the body. New blood vessel growth occurs in response to Vascular Endothelial Growth Factor (VEGF) signaling to vascular endothelial cells. The VEGF signal molecules bind to cell surface receptors and elicit a variety of responses including cell proliferation, migration and survival. Previous studies have shown that nonsteroidal anti-inflammatory drugs (NSAIDs) may affect the signaling involved in angiogenesis. A great deal is known about the mostly inhibitory effects of Aspirin (an NSAID) on angiogenesis, however, the angiogenic responses of endothelial cells exposed to different NSAIDs such as Ibuprofen and Naproxen are less well known. Here, four NSAIDs (Aspirin, Ibuprofen, Naproxen and Salicylate) were tested on Human Umbilical Vascular Endothelial Cells (HUVECs) to determine the drug effects on endothelial cell proliferation, migration, tube formation and cell death. Treatments ranged from normal doses (250 microM) to high doses (500 or 1000 microM). High doses of NSAIDs showed significant decreases in proliferation and tube formation in HUVECs. NSAID treatment also showed a decrease in cell proliferation for high dose Ibuprofen and Salicylate and showed significant effects on tube formation with high dose Salicylate and Aspirin. Addition of VEGF signals appeared to rescue tube formation in HUVECs treated with high dose Aspirin, Salicylate and Ibuprofen but not Naproxen. Overall, NSAIDs showed little effect on angiogenesis at normal doses, but inhibit proliferation, migration, and tube formation at higher doses, and may increase cell death. Cells treated with Naproxen showed different responses relative to the other NSAIDs, suggesting that it may act through different downstream pathways.

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Nonsteroidal Anti-inflammatory Drug Effects on Angiogenic Responses in HUVECs

HUB 302-70

Angiogenesis is the process through which new blood vessels form in the body. New blood vessel growth occurs in response to Vascular Endothelial Growth Factor (VEGF) signaling to vascular endothelial cells. The VEGF signal molecules bind to cell surface receptors and elicit a variety of responses including cell proliferation, migration and survival. Previous studies have shown that nonsteroidal anti-inflammatory drugs (NSAIDs) may affect the signaling involved in angiogenesis. A great deal is known about the mostly inhibitory effects of Aspirin (an NSAID) on angiogenesis, however, the angiogenic responses of endothelial cells exposed to different NSAIDs such as Ibuprofen and Naproxen are less well known. Here, four NSAIDs (Aspirin, Ibuprofen, Naproxen and Salicylate) were tested on Human Umbilical Vascular Endothelial Cells (HUVECs) to determine the drug effects on endothelial cell proliferation, migration, tube formation and cell death. Treatments ranged from normal doses (250 microM) to high doses (500 or 1000 microM). High doses of NSAIDs showed significant decreases in proliferation and tube formation in HUVECs. NSAID treatment also showed a decrease in cell proliferation for high dose Ibuprofen and Salicylate and showed significant effects on tube formation with high dose Salicylate and Aspirin. Addition of VEGF signals appeared to rescue tube formation in HUVECs treated with high dose Aspirin, Salicylate and Ibuprofen but not Naproxen. Overall, NSAIDs showed little effect on angiogenesis at normal doses, but inhibit proliferation, migration, and tube formation at higher doses, and may increase cell death. Cells treated with Naproxen showed different responses relative to the other NSAIDs, suggesting that it may act through different downstream pathways.