Oxidized LDL-Induced Apoptosis

Benoist, Hervé; Salvayre, Robert; Nègre‐Salvayre, Anne

doi:10.1007/0-306-47931-1_7

Cited by 7 publications

(10 citation statements)

References 156 publications

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“…For example, recent evidence suggests that oxidized LDL induces apoptosis both through activation of death receptors and through mitochondrial pathways. It has also recently been reported that the oxysterols, lipid hydroperoxides, oxidized phospholipids, and free cholesterol found within oxidized LDL independently induce death (2,5,11,27,28,30,36,47,50,51,(53)(54)(55). In the present study and in keeping with previous observations, it was found that even very low concentrations of oxidized LDL were capable of inducing markers of apoptosis in the RAW cells, C. pneumoniae is an obligate intracellular pathogen, and as such this organism is dependent on the continued functioning of the host cell to support bacterial growth and the capacity for sustained infection.…”

Section: Discussionmentioning

confidence: 99%

“…Most macrophages within atherosclerotic plaques are converted into foam cells by the unregulated accumulation of lipid. Components of oxidized low-density lipoprotein (ox-LDL) and/or unesterified cholesterol kill cultured macrophages by both apoptotic and nonapoptotic pathways (2,5,11,27,28,30,36,47,50,51,(53)(54)(55). To date, it is not known whether C. pneumoniae infection kills macrophage-derived foam cells and, in turn, contributes to the destabilization of advanced atherosclerotic lesions.…”

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confidence: 99%

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Chlamydia pneumoniaeAugments the Oxidized Low-Density Lipoprotein-Induced Death of Mouse Macrophages by a Caspase-Independent Pathway

Yaraei¹,

Campbell²,

Zhu

et al. 2005

Infect Immun

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Chlamydia pneumoniae is a common respiratory pathogen that is associated with an increased risk of cardiovascular disease. However, the mechanisms by which C. pneumoniae contributes to cardiovascular disease have not been determined yet. C. pneumoniae infection may accelerate the death of cells within atherosclerotic lesions and contribute to the formation of unstable lesions. To test this hypothesis, the impact of C. pneumoniae infection on the death of lipid-loaded mouse macrophages was investigated. It was observed that RAW 264.7 cells are highly susceptible to the toxic effects of oxidized low-density lipoprotein (LDL) and exhibit markers of cell death within 24 h of treatment with as little as 5 g/ml oxidized LDL. Subsequent infection with either live C. pneumoniae or heat-killed or UV-inactivated C. pneumoniae at a low multiplicity of infection for 24 to 72 h stimulated both additional binding of annexin V and the uptake of propidium iodide. Thus, C. pneumoniae augments the effects of oxidized LDL on cell death independent of a sustained infection. However, unlike oxidized LDL, C. pneumoniae infection does not activate caspase 3 or induce formation of the mitochondrial transition pore or the fragmentation of DNA, all of which are classical markers of apoptosis. Furthermore, primary bone marrow macrophages isolated from mice deficient in Toll-like receptor 2 (TLR-2) but not TLR-4 are resistant to C. pneumoniae-induced death. These data suggest that C. pneumoniae kills cells by a caspase-independent pathway and that the process is potentially mediated by activation of TLR-2.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Chlamydia pneumoniaeAugments the Oxidized Low-Density Lipoprotein-Induced Death of Mouse Macrophages by a Caspase-Independent Pathway

Yaraei¹,

Campbell²,

Zhu

et al. 2005

Infect Immun

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“…Ox-LDL can induce apoptosis in a variety of cell types and ox-LDL-mediated apoptosis may participate in the progression of atherosclerosis, and the final acute cardiovascular events171819. Ox-LDL was found to induce severe cell damage and irregular electrical activity in adult ventricular myocytes6.…”

Section: Discussionmentioning

confidence: 99%

Oxidized Low-Density Lipoprotein Induces Apoptosis in Cultured Neonatal Rat Cardiomyocytes by Modulating the TLR4/NF-κB Pathway

Wang

Sun

Yang

et al. 2016

Sci Rep

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This study was designed to investigate the apoptosis induced by oxidized low-density lipoprotein (ox-LDL) in cultured neonatal rat cardiomyocytes and explore the possible mechanisms. We evaluated whether ox-LDL-induced apoptosis depended in part on the activation of toll-like receptor-4(TLR4)/Nuclear factor κB (NF-κB) signaling pathway. Cells were cultivated with and without ox-LDL. Cell apoptosis was evaluated by flow cytometry. Immunofluorescence, western blot analysis and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to assess protein or mRNA expressions. Resatorvid (TAK-242), an exogenous synthetic antagonist for TLR4, was used to inhibit TLR4 signal transduction. Dose- and time-dependent apoptotic index of cardiomyocytes occurred after ox-LDL treatment. Incubation of cardiomyocytes with ox-LDL (50 μg/mL) for 24 hours increased TLR4 and NF-κB expressions significantly. Decrease of Bcl-2/Bax protein ratio, activation of caspase-3 and 9 were also detected. Ox-LDL-induced cardiomyocyte apoptosis, TLR4 and NF-κB expressions were attenuated by pretreatment with TAK-242. In conclusion, our findings indicate that the apoptosis induced by ox-LDL in cultured neonatal rat cardiomyocytes at least in part by modulating the TLR4/NF-κB signaling pathway.

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“…Furthermore, ox-LDL induces migration and proliferation of smooth muscle cells, impedes endothelial cell migration, interferes with endothelium-mediated relaxation, and promotes procoagulant properties of vascular cells by enhancing the expression of tissue factor in endothelial cells, smooth muscle cells, and macrophages (Colles et al 2001). Finally, ox-LDL can induce both apoptosis and necrosis (Martinet and Kockx 2001;Mayr and Xu 2001;Benoist et al 2002;Salvayre et al 2002;Napoli 2003). Although the toxicity of ox-LDL has been recognized for a long time ago, the presence of ox-LDL in the plasma of patients with atherosclerosis was not discovered until recently (Itabe et al 1996;Sattler et al 1998).…”

Section: Endocytosis Of Ox-ldlmentioning

confidence: 99%

Lectin‐like Oxidized Low‐density Lipoprotein Receptor‐1, a New Promising Target for the Therapy of Atherosclerosis?

Chen

Zhang

2007

Cardiovascular Drug Reviews

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Endothelial activation and dysfunction induced by oxidized modified low-density lipoprotein (ox-LDL) is one of the key steps in the initiation of atherosclerosis. Recent studies have shown that a new lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) mediates the recognition and internalization of ox-LDL. LOX-1 is the main receptor for ox-LDL and may play an important role in the pathogenesis of hypertension, diabetes, and, especially, of atherosclerosis. The potential role of LOX-1 in the pathogenesis of atherosclerosis includes: endocytosis of ox-LDL, expression co-location with atherosclerosis enhanced by atherosclerosis-related risk factors, elevated LOX-1 protein in cardiovascular disease, effects related to atherosclerosis and eliminated by antiatherosclerotic drugs. Identification and regulation of LOX-1 and understanding its signal transduction pathways might improve our insight toward the pathogenesis of atherosclerosis and provide a selective treatment approach. LOX-1 might be a potential and promising target for the development of novel antiatherosclerotic drugs. However, due to limited knowledge about LOX-1, there are still many questions to be answered.

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Oxidized LDL-Induced Apoptosis

Cited by 7 publications

References 156 publications

Chlamydia pneumoniaeAugments the Oxidized Low-Density Lipoprotein-Induced Death of Mouse Macrophages by a Caspase-Independent Pathway

Chlamydia pneumoniaeAugments the Oxidized Low-Density Lipoprotein-Induced Death of Mouse Macrophages by a Caspase-Independent Pathway

Oxidized Low-Density Lipoprotein Induces Apoptosis in Cultured Neonatal Rat Cardiomyocytes by Modulating the TLR4/NF-κB Pathway

Lectin‐like Oxidized Low‐density Lipoprotein Receptor‐1, a New Promising Target for the Therapy of Atherosclerosis?

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