Inhibition of cholesterol esterification in rabbit aorta by prostaglandin E2

Berberian, P.A.; Ziboh, Vincent A.; Hsia, S.L.

doi:10.1016/0021-9150(77)90058-2

Cited by 25 publications

(6 citation statements)

References 23 publications

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“…4) [10]. However, PGE2 significantly inhibited ACAT activity by 60%, a finding similar to that reported by Berberian et al [9]. This inhibition occurred in the presence or ab sence of DDA ( fig.…”

Section: Effects Of Arterial Injury On Ce Metabolism and Pgi2 Productsupporting

confidence: 77%

“…E PGI2 A. PGI2 20 80 Because Hajjar et al [10,11], Berberian et al [9], Subbïah [12], and Subbiah and Dicke [13] have demonstrated that eicosanoids can alter CE-metabolizing enzymes, the potential effects of PGI2 and 6-keto PGEi on cholesterol/CE accumulation in arterial smooth muscle cells were examined [11]. These ex periments were of particular interest, since the effects of prostaglandins on enzyme ac tivity may be short-term and not sufficient enough to affect the mass balance of sterols in the cell.…”

Section: Nceh Activity Acat Activitymentioning

confidence: 99%

“…Experimen tal results have shown that enzyme activities involved in arterial CE metabolism may be modulated by several prostaglandins [9][10][11][12][13], other hormones [6], lipoproteins [14,15], and intracellular levels of cyclic nucleotides [10,11], Although the role of PGI2 in hemo stasis has been extensively investigated [16], little is known with regard to the effects of this particular eicosanoid on lipid accumula tion in arterial smooth muscle cells during vascular disease. In this regard, the hypothe sis was tested that PGI2 and several other prostaglandins may directly alter CE hydro lytic and synthetic activities which can, in turn, affect cholesterol and CE accumulation in cultured arterial smooth muscle cells [10, as one would anticipate.…”

Section: Introductionmentioning

confidence: 99%

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Prostaglandins Modulate Arterial Cholesteryl Ester Metabolism

Hajjar¹

1984

Enzyme

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Cholesterol and cholesteryl esters (CE) are the two major classes of lipids which accumulate in arteries during human arteriosclerosis. Mechanisms responsible for this arterial lipid accretion remain to be fully elucidated. In recent years, we have suggested that prostaglandins may have an important role in the modulation of intracellular arterial CE metabolism through their interaction with cyclic nucleotides. This hypothesis was based on observations that arteriosclerotic arteries produce less prostaglandins, particularly prostacyclin, and have altered CE synthetic and hydrolytic activities as compared to uninvolved arteries. This review is a summary of our present knowledge concerning the role of eicosanoids and cyclic nucleotides in the modulation of enzyme activities responsible for arterial CE synthesis and hydrolysis.

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Section: Effects Of Arterial Injury On Ce Metabolism and Pgi2 Productsupporting

confidence: 77%

Section: Nceh Activity Acat Activitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prostaglandins Modulate Arterial Cholesteryl Ester Metabolism

Hajjar¹

1984

Enzyme

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“…5616 " 21 Therefore, a rise in PGE 2 production by the arterial wall could favor the development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…17 Little is yet known concerning PGE 2 production by human arteries; however, PGE 2 may play a role in atherosclerosis since it induces platelet aggregation and can inhibit in vitro cholesterol ester hydrolase activity, thus enhancing lipid deposition in arteries. 5618 " 21 The present study concerns the production of PGI 2 and PGE 2 in human aortas and the possible relationship of these substances to atherogenesis. Previous studies dealing with established lesions have failed to show a relationship to the type of atherosclerosis and PGI 2 production.…”

mentioning

confidence: 99%

Alteration in prostacyclin and prostaglandin E2 production. Correlation with changes in human aortic atherosclerotic disease.

Rolland¹,

Jouve²,

Pellegrin³

et al. 1984

Arteriosclerosis

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Prostacyclin (PGI 2 ) and prostaglandin E 2 (PGE 2 ) production was Investigated in human aortas (five controls and 27 with atherosclerotic lesions). The specific activities of PGI 2 and PGE 2 synthetase were studied using radioimmunoassays of PGE 2 and 6-keto-PGE 1( , of aortic microsomes incubated in the presence of additional substrate and cofactors. The atherosclerotic lesions were examined under the light microscope and were classified as Stage 1 when the disease was restricted to the intima and as Stages 2 and 3 when there were moderate or advanced lesions. Prostaglandin production for the control group (n = 5), Stage 1 (n = 7), Stage 2 (n = 10), and Stage 3 (n = 10) were as follows: 454 ± 15, 162 ± 81, 92 ± 90, and 65 ± 61 pmol 6-K-PGF 1u /50 mg proteln/10 minutes; and 15 ± 12, 399 ± 406, 227 ± 174, and 366 ± 362 pmol PGEj/50 mg protein/10 minutes (mean ± SD) respectively. We conclude that: 1) In normal aortas, PGE 2 production was low, while PGI 2 synthesis activity was elevated. The reverse situation was observed In aortas with atherosclerosis lesions (p < 0.05). 2) There was an inverse relationship between PGE 2 and PGI, production (p < 0.05).3) There was a direct hlstologlc relationship between lower PGI 2 production and atherosclerosis progression. A decided decline In 6-K-PGF,,, production was detected in aortas In the early stages (65% of control values). 4) By contrast, a progressive increase In PGE 2 production was found In Stage 2 and Stage 3 groups (p < 0.05). These results demonstrate that there are correlations between the changes In prostaglandin production and the morphological features of atherosclerosis development. Because of the pharmacologlc properties of prostaglandins, these changes in prostaglandin production may promote the development of atherosclerosis. (Arteriosclerosis 4:70-78, January/February 1984)

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Inhibition of Mitotic and Proliferative Activity of Smooth Muscle Cells by Prostaglandin E1

Sinzinger¹

1986

Prostaglandin E1 in Atherosclerosis

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Inhibition of cholesterol esterification in rabbit aorta by prostaglandin E2

Cited by 25 publications

References 23 publications

Prostaglandins Modulate Arterial Cholesteryl Ester Metabolism

Prostaglandins Modulate Arterial Cholesteryl Ester Metabolism

Alteration in prostacyclin and prostaglandin E2 production. Correlation with changes in human aortic atherosclerotic disease.

Inhibition of Mitotic and Proliferative Activity of Smooth Muscle Cells by Prostaglandin E1

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