Lp(a) and LDL induce apoptosis in human endothelial cells and in rabbit aorta: Role of oxidative stress

Galle, Jan; Schneider, Reinhard; Heinloth, Alexandra N.; Wanner, Christoph; Galle, Peter R.; Conzelmann, Ernst; Dimmeler, Stefanie; Heermeier, Kathrin

doi:10.1046/j.1523-1755.1999.00351.x

Cited by 122 publications

(79 citation statements)

References 52 publications

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“…For example, aortic SMCs obtained from hSod1Tg ϩ/0 and hCatTg ϩ/0 mice, compared with aortic SMCs from their wild-type littermates, showed a 50% decrease in the percentage of cells with DNA fragmentation and a 50% decrease in caspase activity induced by oxLDL. These results are consistent with the observations of Galle et al 9 showing that the addition of SOD or catalase to the culture medium blunted apoptosis induced by oxLDL. In addition, we observed that aortic SMCs obtained from Sod2 ϩ/Ϫ and Gpx1 Ϫ/Ϫ mice showed a significant increase in the percentage of cells with DNA fragmentation and a significant increase in caspase activity compared with wild-type mice.…”

Section: Discussionsupporting

confidence: 93%

“…In addition, we observed that aortic SMCs obtained from Sod2 ϩ/Ϫ and Gpx1 Ϫ/Ϫ mice showed a significant increase in the percentage of cells with DNA fragmentation and a significant increase in caspase activity compared with wild-type mice. Results from Galle et al 9 and from our studies indicate that antioxidant enzymes protect vascular cells from apoptosis induced by oxLDL. Antioxidant enzymes also have been found to protect cells against apoptosis induced by other types of stimuli.…”

Section: Discussionsupporting

confidence: 69%

“…7 Recently, studies have shown that the degree of LDL oxidation is directly proportional to the rate of superoxide production 8 and that oxLDL increases superoxide formation in cultured vascular cells. 9 Thus, cell-mediated LDL oxidation and oxLDL-induced cell death appear to be a reactive oxygen species (ROS)-dependent cycle. Free radicals released from vascular cells mediate oxidation of LDL that enters the arterial wall as a native form; the oxidized forms of LDL, in turn, induce cells to generate more free radicals.…”

mentioning

confidence: 99%

“…The effect of antioxidant enzymes on oxLDL-induced cell death has also been investigated. For example, Galle et al 9 have observed that the presence of exogenous SOD and catalase in culture medium inhibits oxLDL-induced apoptosis in human ECs and rabbit aortic segments.…”

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confidence: 99%

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Changes in Expression of Antioxidant Enzymes Affect Cell-Mediated LDL Oxidation and Oxidized LDL–Induced Apoptosis in Mouse Aortic Cells

Guo

Remmen

Hong

et al. 2001

ATVB

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Abstract-Transgenic mice overexpressing Cu/Zn superoxide dismutase (hSod1Tg ϩ/0 ) or catalase (hCatTg ϩ/0 ) and knockout mice underexpressing manganese superoxide dismutase (Sod2 ϩ/Ϫ ) or glutathione peroxidase-1 (Gpx1 Ϫ/Ϫ ) were used to study the effect of antioxidant enzymes on cell-mediated low density lipoprotein (LDL) oxidation and oxidized LDL (oxLDL)-induced apoptosis. Incubation of LDL with mouse aortic segments or smooth muscle cells (SMCs) resulted in a significant increase in LDL oxidation. However, LDL oxidation was significantly reduced when LDL was incubated with aortic segments and SMCs obtained from hSod1Tg ϩ/0 and hCatTg ϩ/0 mice compared with those obtained from wild-type mice. In contrast, LDL oxidation was significantly increased when LDL was incubated with aortic segments and SMCs obtained from Sod2 ϩ/Ϫ and Gpx1 Ϫ/Ϫ mice. CuSO 4 -oxidized LDL increased DNA fragmentation and caspase activities in the primary cultures of mouse aortic SMCs. However, oxLDL-induced DNA fragmentation and caspase activities were reduced 50% in SMCs obtained from hSod1Tg ϩ/0 and hCatTg ϩ/0 mice compared with wild-type control mice. In contrast, oxLDL-induced DNA fragmentation and caspase activities were significantly increased in SMCs obtained from Sod2 ϩ/Ϫ and Gpx1 Ϫ/Ϫ mice. These findings suggest that overexpression of Cu/Zn superoxide dismutase or catalase reduces cell-mediated LDL oxidation and oxLDL-induced apoptosis, whereas underexpression of manganese superoxide dismutase or glutathione peroxidase-1 increases cell-mediated LDL oxidation and oxLDLinduced apoptosis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 69%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Changes in Expression of Antioxidant Enzymes Affect Cell-Mediated LDL Oxidation and Oxidized LDL–Induced Apoptosis in Mouse Aortic Cells

Guo

Remmen

Hong

et al. 2001

ATVB

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“…2). Las lipoproteínas aterogénicas, especialmente las formas oxidadas, podrían ser las inductoras de la apoptosis de las células endoteliales en el contexto de la aterosclerosis [35][36][37] .…”

Section: Apoptosis De Las Células Endotelialesunclassified

Apoptosis en las enfermedades cardiovasculares

Díez¹

2000

Revista Española de Cardiología

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INTRODUCCIÓNDesde las primeras descripciones clásicas de Virchow se reconocía un tipo de muerte celular: la necrosis. Sin embargo, a finales del siglo pasado, Walter Flemming describió un tipo de muerte celular con características morfológicas diferentes, al que denominó cromatólisis. Tuvo que transcurrir casi un siglo hasta que este tipo de muerte celular fuese adecuadamente caracterizado por Kerr, quien en 1972 propuso el tér-mino apoptosis para denominarlo 1 .En los últimos 20 años, la apoptosis y la necrosis se han considerado como los dos tipos fundamentales de muerte celular. Sin embargo, Majno y Joris han puesto de manifiesto la inconsistencia de este concepto 2 . En efecto, en términos estrictos, la necrosis representa el conjunto de cambios degradativos en los que culmina cualquier tipo de muerte celular. Así, a la necrosis se llega tanto por un proceso de apoptosis, morfológica-mente caracterizado por el arrugamiento y la fragmentación de la célula, como por un proceso de oncosis, en el que la célula se hincha y estalla. Por lo tanto, hoy día cabe distinguir dos tipos fundamentales de muerte celular: el apoptótico y el oncocítico. La apoptosis constituye una forma de muerte celular con características morfológicas y dinámicas distintas de la muerte por oncosis o por necrosis. Desde el punto de vista de la arquitectura celular, la apoptosis equilibra el efecto de la proliferación celular. Por ello, las alteraciones de la regulación de la apoptosis pueden participar en el desarrollo de numerosas enfermedades. Es el caso de la apoptosis exagerada, que conduce a la atrofia y al fallo de la función de un órgano, o de la apoptosis insuficiente, que propicia el remodelado estructural organotisular. En los últimos años se asiste a una gran expansión en la investigación sobre apoptosis, una investigación en la que también participa la comunidad cardiovascular. Desde muy diversos ámbitos de la medicina cardiovascular se han aportado observaciones sobre el posible papel de la apoptosis en síndromes que oscilan desde los defectos de conducción hasta la insuficiencia cardíaca congestiva, desde la aterosclerosis hasta los aneurismas. No hay duda de que esas observaciones puntuales acabarán configurando conceptos etiopatogénicos y fisiopatológi-cos que serán la base del diseño de nuevas estrategias diagnósticas y terapéuticas. A R T Í C U L O D E R E V I S I Ó N

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Anthocyanins and their physiologically relevant metabolites alter the expression of IL‐6 and VCAM‐1 in CD40L and oxidized LDL challenged vascular endothelial cells

Amin

Czank

Raheem

et al. 2015

Molecular Nutrition Food Res

128

119

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ScopeIn vitro and in vivo studies suggest that dietary anthocyanins modulate cardiovascular disease risk; however, given anthocyanins extensive metabolism, it is likely that their degradation products and conjugated metabolites are responsible for this reported bioactivity.Methods and resultsHuman vascular endothelial cells were stimulated with either oxidized LDL (oxLDL) or cluster of differentiation 40 ligand (CD40L) and cotreated with cyanidin‐3‐glucoside and 11 of its recently identified metabolites, at 0.1, 1, and 10 μM concentrations. Protein and gene expression of IL‐6 and VCAM‐1 was quantified by ELISA and RT‐qPCR. In oxLDL‐stimulated cells the parent anthocyanin had no effect on IL‐6 production, whereas numerous anthocyanin metabolites significantly reduced IL‐6 protein levels; phase II conjugates of protocatechuic acid produced the greatest effects (>75% reduction, p ≤ 0.05). In CD40L‐stimulated cells the anthocyanin and its phase II metabolites reduced IL‐6 protein production, where protocatechuic acid‐4‐sulfate induced the greatest reduction (>96% reduction, p ≤ 0.03). Similarly, the anthocyanin and its metabolites reduced VCAM‐1 protein production, with ferulic acid producing the greatest effect (>65% reduction, p ≤ 0.04).ConclusionThese novel data provide evidence to suggest that anthocyanin metabolites are bioactive at physiologically relevant concentrations and have the potential to modulate cardiovascular disease progression by altering the expression of inflammatory mediators.

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Lp(a) and LDL induce apoptosis in human endothelial cells and in rabbit aorta: Role of oxidative stress

Abstract: Atherogenic lipoproteins stimulate O2- formation and induction of apoptosis in HUVECs and RA, and may thereby influence the pathogenesis of atherosclerosis.

Cited by 122 publications

References 52 publications

Changes in Expression of Antioxidant Enzymes Affect Cell-Mediated LDL Oxidation and Oxidized LDL–Induced Apoptosis in Mouse Aortic Cells

Changes in Expression of Antioxidant Enzymes Affect Cell-Mediated LDL Oxidation and Oxidized LDL–Induced Apoptosis in Mouse Aortic Cells

Apoptosis en las enfermedades cardiovasculares

Anthocyanins and their physiologically relevant metabolites alter the expression of IL‐6 and VCAM‐1 in CD40L and oxidized LDL challenged vascular endothelial cells

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