Control of capillary formation by membrane-anchored extracellular inhibitor of phospholipase A2

W. M. Chen; J. Soria; C. Soria; M. Krimsky; S. Yedgar

doi:10.1016/S0014-5793(02)02907-1

Control of capillary formation by membrane-anchored extracellular inhibitor of phospholipase A₂

W. M. Chen, J. Soria, C. Soria, M. Krimsky, S. Yedgar

Racah Institute of Physics

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Secretory phospholipase A₂ (sPLA₂) has been reported to be involved in cell proliferation in general and in endothelial cell migration, processes required for capillary formation. Subsequently, we examined the potential control of angiogenesis by sPLA₂ inhibition, using a cell-impermeable sPLA₂ inhibitor composed of N-derivatized phosphatidyl-ethanolamine linked to hyaluronic acid. This inhibitor effectively inhibits the proliferation and migration of human bone marrow endothelial cells in a dose-dependent manner, and suppresses capillary formation induced by growth factors involved in vascularization of tumors and of atherosclerotic plaques. It is proposed that sPLA₂ inhibition introduces a novel approach in the control of cancer development and atherosclerosis.

Original language	English
Pages (from-to)	113-118
Number of pages	6
Journal	FEBS Letters
Volume	522
Issue number	1-3
DOIs	https://doi.org/10.1016/S0014-5793(02)02907-1
State	Published - 3 Jul 2002

Keywords

Angiogenesis
Antiangiogenic therapy
Endothelial cell
Extracellular phospholipase A inhibitor

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0014-5793(02)02907-1

Cite this

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abstract = "Secretory phospholipase A2 (sPLA2) has been reported to be involved in cell proliferation in general and in endothelial cell migration, processes required for capillary formation. Subsequently, we examined the potential control of angiogenesis by sPLA2 inhibition, using a cell-impermeable sPLA2 inhibitor composed of N-derivatized phosphatidyl-ethanolamine linked to hyaluronic acid. This inhibitor effectively inhibits the proliferation and migration of human bone marrow endothelial cells in a dose-dependent manner, and suppresses capillary formation induced by growth factors involved in vascularization of tumors and of atherosclerotic plaques. It is proposed that sPLA2 inhibition introduces a novel approach in the control of cancer development and atherosclerosis.",

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