Modulation of angiogenic processes in cultured endothelial cells by low density lipoproteins subfractions from patients with familial hypercholesterolemia

Ming Hong Tai, Shiao Mei Kuo, Hui Ting Liang, Kuan Rau Chiou, Hing Chung Lam, Ching Mei Hsu, Henry J. Pownall, Hsin Hung Chen, Max T. Huang, Chao Yuh Yang

研究成果: 雜誌貢獻文章

30 引文 (Scopus)

摘要

Objective: Electronegative low density lipoprotein (LDL) subfractions are cytotoxic to endothelial cells. To continue our study of homozygotic familial hypercholesterolemic (FH)-LDL, we report the effects of FH-LDL subfractions (FH-L1 to FH-L5) on the angiogenic processes in cultured endothelial cells. Methods and results: Subconfluent bovine aortic endothelial cells (BAEC) were treated with LDL subfractions (20 μg/ml), and the effects on angiogenic functions, including cell proliferation, migration, apoptosis, tube formation, secretion of matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF) were determined. The electronegative FH-L4 and FH-L5 inhibited cell proliferation while the other FH-LDL subfractions and LDL from normocholesterolemic subjects (N-LDL) had negligible effects. Like Cu2+ ox-LDL, FH-L5 strongly inhibited endothelial cell viability and FH-L4 had a milder effects. Similarly, FH-L4 and FH-L5 but not the other subfractions retarded cell migration, induced cell apoptosis, and perturbed tube formation by BAEC in matrigel. FH-L5 inhibited secretion of MMP-2 and MMP-9 by BAEC without affecting their endogenous levels. In contrast, FH-L5 increased the VEGF expression in endothelial cells. Conclusions: Our results show for the first time that FH-L5, a circulating LDL subfraction from hypercholesterolemic patients, modulates various angiogenic processes, thereby dysregulating endothelial function in a way that may be atherogenic.
原文英語
頁(從 - 到)448-457
頁數10
期刊Atherosclerosis
186
發行號2
DOIs
出版狀態已發佈 - 六月 1 2006
對外發佈Yes

指紋

Hyperlipoproteinemia Type II
LDL Lipoproteins
Cultured Cells
Endothelial Cells
Cell Count
Vascular Endothelial Growth Factor A
Cell Movement
Cell Proliferation
Apoptosis
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Matrix Metalloproteinases
Cell Survival

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

引用此文

Modulation of angiogenic processes in cultured endothelial cells by low density lipoproteins subfractions from patients with familial hypercholesterolemia. / Tai, Ming Hong; Kuo, Shiao Mei; Liang, Hui Ting; Chiou, Kuan Rau; Lam, Hing Chung; Hsu, Ching Mei; Pownall, Henry J.; Chen, Hsin Hung; Huang, Max T.; Yang, Chao Yuh.

於: Atherosclerosis, 卷 186, 編號 2, 01.06.2006, p. 448-457.

研究成果: 雜誌貢獻文章

Tai, Ming Hong ; Kuo, Shiao Mei ; Liang, Hui Ting ; Chiou, Kuan Rau ; Lam, Hing Chung ; Hsu, Ching Mei ; Pownall, Henry J. ; Chen, Hsin Hung ; Huang, Max T. ; Yang, Chao Yuh. / Modulation of angiogenic processes in cultured endothelial cells by low density lipoproteins subfractions from patients with familial hypercholesterolemia. 於: Atherosclerosis. 2006 ; 卷 186, 編號 2. 頁 448-457.
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abstract = "Objective: Electronegative low density lipoprotein (LDL) subfractions are cytotoxic to endothelial cells. To continue our study of homozygotic familial hypercholesterolemic (FH)-LDL, we report the effects of FH-LDL subfractions (FH-L1 to FH-L5) on the angiogenic processes in cultured endothelial cells. Methods and results: Subconfluent bovine aortic endothelial cells (BAEC) were treated with LDL subfractions (20 μg/ml), and the effects on angiogenic functions, including cell proliferation, migration, apoptosis, tube formation, secretion of matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF) were determined. The electronegative FH-L4 and FH-L5 inhibited cell proliferation while the other FH-LDL subfractions and LDL from normocholesterolemic subjects (N-LDL) had negligible effects. Like Cu2+ ox-LDL, FH-L5 strongly inhibited endothelial cell viability and FH-L4 had a milder effects. Similarly, FH-L4 and FH-L5 but not the other subfractions retarded cell migration, induced cell apoptosis, and perturbed tube formation by BAEC in matrigel. FH-L5 inhibited secretion of MMP-2 and MMP-9 by BAEC without affecting their endogenous levels. In contrast, FH-L5 increased the VEGF expression in endothelial cells. Conclusions: Our results show for the first time that FH-L5, a circulating LDL subfraction from hypercholesterolemic patients, modulates various angiogenic processes, thereby dysregulating endothelial function in a way that may be atherogenic.",
keywords = "Angiogenesis, Apoptosis, Electronegative LDL, Endothelial cell, Matrix metalloproteinase",
author = "Tai, {Ming Hong} and Kuo, {Shiao Mei} and Liang, {Hui Ting} and Chiou, {Kuan Rau} and Lam, {Hing Chung} and Hsu, {Ching Mei} and Pownall, {Henry J.} and Chen, {Hsin Hung} and Huang, {Max T.} and Yang, {Chao Yuh}",
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T1 - Modulation of angiogenic processes in cultured endothelial cells by low density lipoproteins subfractions from patients with familial hypercholesterolemia

AU - Tai, Ming Hong

AU - Kuo, Shiao Mei

AU - Liang, Hui Ting

AU - Chiou, Kuan Rau

AU - Lam, Hing Chung

AU - Hsu, Ching Mei

AU - Pownall, Henry J.

AU - Chen, Hsin Hung

AU - Huang, Max T.

AU - Yang, Chao Yuh

PY - 2006/6/1

Y1 - 2006/6/1

N2 - Objective: Electronegative low density lipoprotein (LDL) subfractions are cytotoxic to endothelial cells. To continue our study of homozygotic familial hypercholesterolemic (FH)-LDL, we report the effects of FH-LDL subfractions (FH-L1 to FH-L5) on the angiogenic processes in cultured endothelial cells. Methods and results: Subconfluent bovine aortic endothelial cells (BAEC) were treated with LDL subfractions (20 μg/ml), and the effects on angiogenic functions, including cell proliferation, migration, apoptosis, tube formation, secretion of matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF) were determined. The electronegative FH-L4 and FH-L5 inhibited cell proliferation while the other FH-LDL subfractions and LDL from normocholesterolemic subjects (N-LDL) had negligible effects. Like Cu2+ ox-LDL, FH-L5 strongly inhibited endothelial cell viability and FH-L4 had a milder effects. Similarly, FH-L4 and FH-L5 but not the other subfractions retarded cell migration, induced cell apoptosis, and perturbed tube formation by BAEC in matrigel. FH-L5 inhibited secretion of MMP-2 and MMP-9 by BAEC without affecting their endogenous levels. In contrast, FH-L5 increased the VEGF expression in endothelial cells. Conclusions: Our results show for the first time that FH-L5, a circulating LDL subfraction from hypercholesterolemic patients, modulates various angiogenic processes, thereby dysregulating endothelial function in a way that may be atherogenic.

AB - Objective: Electronegative low density lipoprotein (LDL) subfractions are cytotoxic to endothelial cells. To continue our study of homozygotic familial hypercholesterolemic (FH)-LDL, we report the effects of FH-LDL subfractions (FH-L1 to FH-L5) on the angiogenic processes in cultured endothelial cells. Methods and results: Subconfluent bovine aortic endothelial cells (BAEC) were treated with LDL subfractions (20 μg/ml), and the effects on angiogenic functions, including cell proliferation, migration, apoptosis, tube formation, secretion of matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF) were determined. The electronegative FH-L4 and FH-L5 inhibited cell proliferation while the other FH-LDL subfractions and LDL from normocholesterolemic subjects (N-LDL) had negligible effects. Like Cu2+ ox-LDL, FH-L5 strongly inhibited endothelial cell viability and FH-L4 had a milder effects. Similarly, FH-L4 and FH-L5 but not the other subfractions retarded cell migration, induced cell apoptosis, and perturbed tube formation by BAEC in matrigel. FH-L5 inhibited secretion of MMP-2 and MMP-9 by BAEC without affecting their endogenous levels. In contrast, FH-L5 increased the VEGF expression in endothelial cells. Conclusions: Our results show for the first time that FH-L5, a circulating LDL subfraction from hypercholesterolemic patients, modulates various angiogenic processes, thereby dysregulating endothelial function in a way that may be atherogenic.

KW - Angiogenesis

KW - Apoptosis

KW - Electronegative LDL

KW - Endothelial cell

KW - Matrix metalloproteinase

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U2 - 10.1016/j.atherosclerosis.2005.08.022

DO - 10.1016/j.atherosclerosis.2005.08.022

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SP - 448

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JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

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