Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells

Jaw Wen Chen; Feng Yen Lin; Yung Hsiang Chen; Tao Cheng Wu; Yuh Lien Chen; Shing Jong Lin

doi:10.1161/01.ATV.0000145016.69181.fa

Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells

Jaw Wen Chen, Feng Yen Lin, Yung Hsiang Chen, Tao Cheng Wu, Yuh Lien Chen, Shing Jong Lin

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

48 Citations (Scopus)

Abstract

Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P

Original language	English
Pages (from-to)	2075-2081
Number of pages	7
Journal	Arteriosclerosis, Thrombosis, and Vascular Biology
Volume	24
Issue number	11
DOIs	https://doi.org/10.1161/01.ATV.0000145016.69181.fa
Publication status	Published - Nov 2004
Externally published	Yes

Keywords

Antioxidant
Atherosclerosis
Carvedilol
Cell adhesion molecules
Endothelium

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

UN SDGs

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

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10.1161/01.ATV.0000145016.69181.fa

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Chen, J. W., Lin, F. Y., Chen, Y. H., Wu, T. C., Chen, Y. L., & Lin, S. J. (2004). Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells. Arteriosclerosis, Thrombosis, and Vascular Biology, 24(11), 2075-2081. https://doi.org/10.1161/01.ATV.0000145016.69181.fa

Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells. / Chen, Jaw Wen ; Lin, Feng Yen; Chen, Yung Hsiang et al.
In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 24, No. 11, 11.2004, p. 2075-2081.

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

Chen, JW , Lin, FY, Chen, YH, Wu, TC, Chen, YL & Lin, SJ 2004, 'Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells', Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 24, no. 11, pp. 2075-2081. https://doi.org/10.1161/01.ATV.0000145016.69181.fa

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abstract = "Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P",

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author = "Chen, {Jaw Wen} and Lin, {Feng Yen} and Chen, {Yung Hsiang} and Wu, {Tao Cheng} and Chen, {Yuh Lien} and Lin, {Shing Jong}",

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AU - Chen, Jaw Wen

AU - Lin, Feng Yen

AU - Chen, Yung Hsiang

AU - Wu, Tao Cheng

AU - Chen, Yuh Lien

AU - Lin, Shing Jong

PY - 2004/11

Y1 - 2004/11

N2 - Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P

AB - Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P

KW - Antioxidant

KW - Atherosclerosis

KW - Carvedilol

KW - Cell adhesion molecules

KW - Endothelium

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Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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