Suppression of foam cell lesions in hypercholesterolemic rabbits by inhibition of thromboxane A2 synthesis.

Skrinska, Victor; Konieczkowski, Martha; Gerrity, Ross G.; Galang, Cirilio F.; Rebec, Mihailo V.

doi:10.1161/01.atv.8.4.359

Cited by 27 publications

(9 citation statements)

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“…In the present study, as expected, all the animals rapidly (36), polyunsaturated oils (37), and probucol (38,39). It has also been reported that intravenous administration of large amounts of dispersed phospholipids (0.5-3.5 g two to three times a week) induces regression of experimental atherosclerosis in rabbits (39)(40)(41).…”

Section: Discussionsupporting

confidence: 88%

Regression of atherosclerotic lesions by high density lipoprotein plasma fraction in the cholesterol-fed rabbit.

Badimón¹,

Badimón²,

Fuster³

1990

J. Clin. Invest.

726

365

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The effects of homologous plasma HDL and VHDL fractions on established atherosclerotic lesions were studied in cholesterol-fed rabbits. Atherosclerosis was induced by feeding the animals a 0.5% cholesterol-rich diet for 60 d (group 1). Another group of animals were maintained on the same diet for 90 d (group 2). A third group was also fed the same diet for 90 d but received 50 mg HDL-VHDL protein per wk (isolated from normolipemic rabbit plasma) during the last 30 d (group 3). Aortic atherosclerotic involvement at the completion of the study was 34±4% in group 1, 38.8±5% in group 2, and 17.8±4% in group 3 (P < 0.005). Aortic lipid deposition was also significantly reduced in group 3 compared with group 1 (studied at only 60 d) and group 2. This is the first in vivo, prospective evidence of the antiatherogenic effect of HDL-VHDL against preexisting atherosclerosis. Our results showed that HDL plasma fractions were able to induce regression of established aortic fatty streaks and lipid deposits. Our results suggest that it may be possible not only to inhibit progression but even to reduce established atherosclerotic lesions by HDL administration. (J. Clin. Invest. 1990.

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Section: Discussionsupporting

confidence: 88%

Regression of atherosclerotic lesions by high density lipoprotein plasma fraction in the cholesterol-fed rabbit.

Badimón¹,

Badimón²,

Fuster³

1990

J. Clin. Invest.

726

365

View full text Add to dashboard Cite

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“…The physiological basis of this action may be related not only to the cholesterol-lowering A B C effects of policosanol, but also to the reduction of thromboxane A 2 (TxA 2 ) and to the increase in prostacyclin levels induced by policosanol (30). Skrinska et al (31) showed that rabbits fed a hypercholesterolemic diet and treated with a thromboxane synthetase inhibitor (UK-38485) developed significantly fewer lesions due to foam cells than those fed the atherogenic diet only. It has been also reported that BM 13505, a specific TxA 2 antagonist, has an antiatherogenic effect by reducing the deposition of cholesterol on the arterial wall and by retarding plaque formation in coronary arteries of cholesterol-fed rabbits (32).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of policosanol on atherosclerotic lesions in rabbits with exogenous hypercholesterolemia

Arruzazabala¹,

Noa²,

Menéndez³

et al. 2000

Braz J Med Biol Res

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Policosanol is a mixture of higher aliphatic alcohols purified from sugar cane wax, with cholesterol-lowering effects demonstrable in experimental models and in patients with type II hypercholesterolemia. The protective effects of policosanol on atherosclerotic lesions experimentally induced by lipofundin in rabbits and rats and spontaneously developed in stumptail monkeys have been described. The present study was conducted to determine whether policosanol administered orally to rabbits with exogenous hypercholesterolemia also protects against the development of atherosclerotic lesions. Male New Zealand rabbits weighing 1.5 to 2 kg were randomly divided into three experimental groups which received 25 or 200 mg/kg policosanol (N = 7) orally for 60 days with acacia gum as vehicle or acacia gum alone (control group, N = 9). All animals received a cholesterol-rich diet (0.5%) during the entire period. Control animals developed marked hypercholesterolemia, macroscopic lesions and arterial intimal thickening. Intima thickness was significantly less (32.5 ± 7 and 25.4 ± 4) in hypercholesterolemic rabbits treated with policosanol than in controls (57.6 ± 9). In most policosanol-treated animals, atherosclerotic lesions were not present, and in others, thickness of fatty streaks had less foam cell layers than in controls. We conclude that policosanol has a protective effect on the atherosclerotic lesions occurring in this experimental model.

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“…Thus, 4E-BPs in hibit only cap-dependent translation initiation and have no effect on the cap-independent translation initiation , whereas NATl represses both types of translation initiation. Perhaps more important, the limited number of cellular mRNAs translated by the cap-independent mechanisms all encode proteins with important cellular functions, such as fibroblast growth factor 2 (Skrinska et al 1988), insulin growth factor II (Teerink et al 1995), and eIF4G (Gan and Rhoads 1996). Therefore, the repression of this type of translation by NATl may have a great impact.…”

Section: ^^1^mentioning

confidence: 99%

A novel translational repressor mRNA is edited extensively in livers containing tumors caused by the transgene expression of the apoB mRNA-editing enzyme.

Yamanaka¹,

Poksay²,

Arnold³

et al. 1997

Genes Dev.

214

213

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Transgene expression of the apoUpoprotein B mRNA-editing enzyme (APOBEC-1) causes dysplasia and carcinoma in mouse and rabbit livers. Using a modified differential display technique, we identified a novel mRNA (NATl for novel APOBEC-1 target no. 1) that is extensively edited at multiple sites in these livers. The aberrant editing alters encoded amino acids, creates stop codons, and results in markedly reduced levels of the NATl protein in transgenic mouse livers. NATl is expressed ubiquitously and is extraordinarily conserved among species. It has homology to the carboxy-terminal portion of the eukaryotic translation initiation factor (elF) 4G that binds eIF4A and eIF4E to form eIF4F. NATl binds eIF4A but not eIF4E and inhibits both cap-dependent and cap-independent translation. NATl is likely to be a fundamental translational repressor, and its aberrant editing could contribute to the potent oncogenesis induced by overexpression of APOBEC-1.

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Suppression of foam cell lesions in hypercholesterolemic rabbits by inhibition of thromboxane A2 synthesis.

Cited by 27 publications

References 0 publications

Regression of atherosclerotic lesions by high density lipoprotein plasma fraction in the cholesterol-fed rabbit.

Regression of atherosclerotic lesions by high density lipoprotein plasma fraction in the cholesterol-fed rabbit.

Protective effect of policosanol on atherosclerotic lesions in rabbits with exogenous hypercholesterolemia

A novel translational repressor mRNA is edited extensively in livers containing tumors caused by the transgene expression of the apoB mRNA-editing enzyme.

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