Effect of Lipoprotein on In Vitro Synthesis of DNA in Aortic Tissue

Augustyn, Joan M.; Ke, Fritz; As, Daoud; Jarmolych, J.

doi:10.1007/978-1-4613-4220-5_53

Cited by 4 publications

(5 citation statements)

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“…LDL (d < 1.030) isolated from normolipemic human serum stimulated the growth of aortic SMC (Fless et al, 1982). In contrast, LDL (d 1.019-1.063) and HDL (d 1.063-1.21) isolated from both normocholesterolemic and hypercholesterolemic porcine sera had no effect on the growth of porcine aortic SMC (Augustyn et al, 1977). To date, there is little comparative study of the effects of lipoproteins on the proliferation of human adult EC and SMC.…”

mentioning

confidence: 67%

Role of lipoproteins in growth of human adult arterial endothelial and smooth muscle cells in low lipoprotein‐deficient serum

Chen

Hoshi

McClure

et al. 1986

Journal Cellular Physiology

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Recently improved culture conditions for human adult arterial endothelial and smooth muscle cells from a wide variety of donors have been used to study the effects of lipoproteins on proliferation of both cell types in low serum culture medium. Optimal growth of endothelial and smooth muscle cells in an optimal nutrient medium (MCDB 107) containing epidermal growth factor, a partially purified fraction from bovine brain, and 1% (v/v) lipoprotein-deficient serum was dependent on either high- or low-density lipoprotein. High- and low-density lipoprotein stimulated cell growth by three- and five-fold, respectively, over a 6-day period. Optimal stimulation of both endothelial and smooth muscle cell growth occurred between 20 and 60 micrograms/ml of high- and low-density lipoproteins, respectively. No correlation between the activation of 3-hydroxyl-3-methylglutaryl coenzyme. A reductase activity and lipoprotein-stimulated cell proliferation was observed. Lipid-free total apolipoproteins or apolipoprotein C peptides from high-density lipoprotein were partially effective and together with oleic acid effectively replaced native high-density lipoprotein for the support of endothelial cell growth. In contrast, apolipoproteins or apolipoprotein C peptides from high-density lipoprotein alone or with oleic acid had no effect on smooth muscle cell proliferation. The results suggest a functional role of high- and low-density lipoproteins and apolipoproteins in the proliferation of human adult endothelial and smooth muscle cells.

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mentioning

confidence: 67%

Role of lipoproteins in growth of human adult arterial endothelial and smooth muscle cells in low lipoprotein‐deficient serum

Chen

Hoshi

McClure

et al. 1986

Journal Cellular Physiology

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“…Likewise low-density lipoprotein (density < 1.030 grdml) isolated from normolipemic human serum has been reported to be mitogenic for smooth muscle cells (Fless et al, 1982). However, VLDL (density < 1.006 gm/mU, LDL (density 1.019-1.063 grdml), and HDL (density 1.063-1.21 gm/ml) isolated from both normocholesterolemic and hypercholesterolemic porcine sera showed no effect on the growth of porcine aortic smooth muscle cells (Augustyn et al, 1977).…”

Section: Discussionmentioning

confidence: 97%

“…In these experiments, the lipoproteins probably potentiated growth factors present in the serum (e.g., PDGF). In the experiments of Augustyn et al (1977), lipoproteins probably failed to increase cell growth because the cells were incubated in unsupplemented serum-free medium that lacked bona fide mitogens required to initiate division.…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have suggested that lipoproteins are mitogenic for these cells (Ross and Glomset, 1973;Fless et al, 1982). Others have shown little or no mitogenic effect (Augustyn et al, 1977). This example is of considerable medical interest in view of the well established pathogenic roles of lipoproteins and smooth muscle proliferation in vascular disease (Ross, 1981).…”

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confidence: 98%

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Lipoproteins increase growth of mitogen‐stimulated arterial smooth muscle cells

Libby¹,

Miao²,

Ordovás³

et al. 1985

Journal Cellular Physiology

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The relationship between lipoproteins and growth of aortic smooth muscle cells has been a matter of controversy. We therefore reexamined this issue using serum-free defined media methodology. By themselves, LDL or HDL (50-500 micrograms/ml) from normolipemic human or bovine plasma produced little or no growth of homologous aortic smooth muscle cells incubated in serum-free medium that was supplemented with insulin and transferrin to maintain cell viability. In fact, LDL prepared in the absence of an antioxidant (BHT) was toxic to these cells. However, in the presence of maximally effective concentrations of platelet-derived growth factor (PDGF), LDL or HDL consistently increased the growth of homologous smooth muscle cells (up to twofold increased in DNA accumulation in 48 hr). Lipoproteins also augmented the growth response of arterial smooth muscle cells to fibroblast growth factor or epidermal growth factor. The mechanism of this effect was investigated further with HDL, because, in contrast to LDL, HDL apoproteins are water-soluble. Neither HDL delipidated by solvent extraction (apoHDL), purified bovine apoA-I, nor cholesterol added in the form of phospholipid vesicles appreciably increased PDGF-induced growth of bovine smooth muscle cells. However, HDL-like particles reconstituted by sonication of apoHDL with cholesterol and phospholipids did increase the growth of cultures of bovine smooth muscle cells treated with PDGF. Uptake of tritiated thymidine by cultures incubated with partially purified PDGF alone (10 micrograms/ml) was 5,693 +/- 235 dpm/24 hr compared to 10,381 +/- 645 dpm/24 hr (p less than 0.01) in the presence of both PDGF and reconstituted HDL-like particles (250 micrograms protein/ml). Thus both the lipid and protein components of HDL may be necessary for optimal potentiation of growth of mitogen-stimulated cells. These results indicate that lipoproteins from normolipemic sera are not bona fide growth factors but can potentiate the growth of mitogen-stimulated cells, perhaps by supplying exogenous cholesterol required for membrane biogenesis. This finding might be important in arterial injury when the release of PDGF and exposure to plasma lipoproteins could act in concert to stimulate the proliferation of smooth muscle cells.

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“…It has been known for many years that the addition of LDL to smooth muscle cells augments the mitogenic effects of serum. [129][130][131] More recently, it has been demonstrated that oxidized LDL is even more effective than is LDL at stimulating both smooth muscle cell and macrophage proliferation in vitro. [132][133][134][135] As vitamin E can block the stimulatory effects of oxidized LDL in smooth muscle cells, 133 this suggests that intracellular oxidative mechanisms play a role in inducing the mitogenic response.…”

Section: Effects Of Oxidative Stress On Cellular Proliferationmentioning

confidence: 99%

Inflammation, Lipids, and Free Radicals: Lessons Learned from the Atherogenic Process

Me¹

1998

Semin Reprod Med

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This review focuses on the question of how oxidative stress in cells populating atherosclerotic lesions stimulates gene expression, cell proliferation, and cell death, and how these events contribute to the initiation, progression, and destablization of the lesions. It is hypothesized that oxidative stress in endothelial cells, macrophages, and smooth muscle cells occurs as a result of the depletion of the cellular content of reduced glutathione. Glutathione becomes oxidized in response to the accumulation of oxidized lipids, the formation of reactive oxygen species released from the mitochondria and generated as part of the activation-induced respiratory burst, and the generation of nitric oxide, peroxynitrite, and thiol radicals. Both in vitro and in vivo evidence suggests that these cells can take up modified lipoproteins that become trapped within the artery wall leading to the overaccumulation of oxidized fatty acids and oxidized forms of cholesterol. The cells also generate oxidized lipids via the activity of lipoxygenases, cyclooxygenases, and myeloperoxidase. A sublethal oxidative stress can activate redox-sensitive kinase cascades and transcription factors such as NFB and AP-1, with resulting increases in the expression of factors associated with an inflammatory response and cellular proliferation. There is also accumulating evidence that suggests that oxidative stress may be associated with the induction of cell death either via stimulation of apoptosis and/or necrosis and that increased cell death contributes to the formation of a necrotic core, the hallmark of an advanced, unstable lesion.

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Effect of Lipoprotein on In Vitro Synthesis of DNA in Aortic Tissue

Cited by 4 publications

References 10 publications

Role of lipoproteins in growth of human adult arterial endothelial and smooth muscle cells in low lipoprotein‐deficient serum

Role of lipoproteins in growth of human adult arterial endothelial and smooth muscle cells in low lipoprotein‐deficient serum

Lipoproteins increase growth of mitogen‐stimulated arterial smooth muscle cells

Inflammation, Lipids, and Free Radicals: Lessons Learned from the Atherogenic Process

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