LDL-induced cytotoxicity and its inhibition by HDL in human vascular smooth muscle and endothelial cells in culture

Hessler, James R.; Robertson, Abel L.; Chisolm, Guy M.

doi:10.1016/0021-9150(79)90166-7

Cited by 485 publications

(209 citation statements)

References 43 publications

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“…In vitro studies had already shown that oxLDL exhibit cytotoxic e ects on cultured endothelial cells, but the type of cell death elicited remained unknown (Hessler et al, 1979). However, several authors recently reported increased apoptotic cell death of bovine aortic endothelial cells exposed to cholesterol oxides in culture (Lizard et al, 1996) and increased apoptosis (and possibly secondary necrosis) of HUVEC after exposure to oxLDL (Dimmeler et al, 1997a;Escargueil-Blanc et al, 1997).…”

Section: Induction Of Pro-apoptotic Pathwaysmentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

304

214

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Apoptotic death has now been recognized in a number of common and threatening vascular diseases, including atherosclerosis. Interest in apoptosis research relates to the fact that apoptosis, in contrast to oncosis, is a highly regulated process of cell death which raises the hope for the development of speci®c therapeutic strategies to alter disease progression. This review summarizes the mechanisms involved in vascular endothelial and smooth muscle cell survival/apoptosis, and the potential roles of apoptotic death in atherosclerosis and restenosis. The potential e ects of modulation of apoptosis in these diseases are also discussed.

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Section: Induction Of Pro-apoptotic Pathwaysmentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

304

214

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“…LDL can undergo postseeretory modifications resulting from oxidation induced by cells and/or by transition metal ions which induce apoB alterations and lipid peroxidation [2,[5][6][7]. Recent studies suggest that oxidized LDL are involved in the genesis of atherosclerotic lesions [3][4][5][6][7]: (i) apoB alterations result in reduced LDL uptake through the apoB/E-receptor mediated pathway and enhanced uptake through the scavenger-receptor pathway ofmacrophages, leading to 'foam' cell formation (characteristic of the early lesions of atheroma) [1,5]; (ii) lipid peroxidation of LDL [3,6,7] results in a cytotoxic effect towards cultured cells [8][9][10][11]. Such cytotoxic events seem to be involved in the progression of the vascular lesions of atherosclerosis, i.e.…”

Section: Introductionmentioning

confidence: 99%

A delayed and sustained rise of cytosolic calcium is elicited by oxidized LDL in cultured bovine aortic endothelial cells

et al. 1992

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Bovine aortic endothelial c~lls (BAEC) pulsed for 5 h with mildly oxidized low density lipoproteins (LDL), exhibit~ a broad, sustained and high peak of [Ca:*]l occurring several hours after the end of the pulse and reachilll~ very high [Ca"+]t values (around 2500--3000 nmol/I) and a concomitant drop of eytosolic pH (around 0.2-0.3 pH units) without any loss of cell viability. When BAEC were continuously pulsed with oxidized LDL, the peak of [Ca2*]~ was more sustained than in short pulse experiments and was associated with irreversible morphological ~hanges usually associat~l with cytotoxi¢ events (blebbin$) and with a marked loss of viability. The potential involvement of thes, biochemical and morphological changes in atherogenesis are discussed.

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“…Purified low density lipoprotein (LDL) was shown to be cytotoxic for endothelial cells by an in vitro assay similar to the 3H-thyrnidine incorporation assay utilized in this study (26). It is known that 60% of patients with PSS have a low density lipoprotein in their serum that precipitates with synthetic polynucleotides, suggesting the LDL may have an immunomodulatory role in scleroderma (27).…”

Section: Discussionmentioning

confidence: 95%

Cytotoxicity of sera from patients with scleroderma

Cohen

Johnson

Hurd

1983

Arthritis & Rheumatism

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Sera from patients with progressive systemic sclerosis were compared with sera from normal individuals and from patients with other connective tissue diseases for cytotoxic effects on cultured human cells. More than 40% of the sera from patients with active progressive systemic sclerosis were cytotoxic by several criteria for pulmonary arterial or umbilical venous endothelial cells, foreskin fibroblasts, and neuroblastoma cells. Cytotoxic sera caused morphologic changes, uptake of trypan blue dye, and a decrease in the incorporation of 'H-thymidine into DNA. In contrast, only 4 sera from normal individuals or patients with other rheumatic diseases affected cell morphology, staining, or uptake of 3H-thymidine. Partial characterization of the cytotoxic factor indicated that it is sensitive to proteolysis by trypsin. The molecular weight of the factor was estimated to be similar to that of albumin.Progressive systemic sclerosis (PSS), or scleroderma, is characterized by alterations in connective tissue composition of skin and visceral organs, but the ~

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LDL-induced cytotoxicity and its inhibition by HDL in human vascular smooth muscle and endothelial cells in culture

Cited by 485 publications

References 43 publications

Apoptosis in the vasculature: mechanisms and functional importance

Apoptosis in the vasculature: mechanisms and functional importance

A delayed and sustained rise of cytosolic calcium is elicited by oxidized LDL in cultured bovine aortic endothelial cells

Cytotoxicity of sera from patients with scleroderma

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