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Query: UMLS:C0004153 (
atherosclerosis
)
77,401
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Estrogen
is known to retard the development of
atherosclerosis
and to work in the brain, but the mechanism of hormonal action is completely unknown. We investigated the effect of estrogen on the activity of neuronal constitutive nitric oxide synthase (NNOS). A low concentration of estrogen (10(-10)(-7) M) enhanced the activity of homogenates of the cytosol fraction of rabbit cerebellums and also that of partially purified NNOS, and high dose (10(-6)(-5) M) attenuated them. The study using estrogen receptor antagonists, tamoxifen, clomiphene, and ICI182780 suggested that estrogen receptor did not relate significantly to those effects of 17 beta-estradiol. 17 alpha-estradiol or progesterone did not change significantly it in low doses, although moderately inhibited it in high doses.
Estrogen
enhanced the fluorescence of dansyl-calmodulin in low doses and attenuated it in high doses, suggesting that estrogen affects Ca(2+)-calmodulin directly. This study demonstrated that estrogen has a biphasic effect on the activity of NNOS through a Ca(2+)-calmodulin.
...
PMID:Biphasic effect of estrogen on neuronal constitutive nitric oxide synthase via Ca(2+)-calmodulin dependent mechanism. 752 39
The prevalence of coronary artery disease is lower in women than in men. Ovarian estrogen is believed to decrease the risk of coronary heart disease. Today, there is an increasing demand for estrogen replacement not only for amelioration of menopausal subjective symptoms but also for the prophylactic action of estrogen against osteoporosis in postmenopausal women. Is generally agreed that estrogen replacement therapy reduces cardiovascular morbidity and mortality in postmenopausal women.
Estrogen
replacement therapy may protect against coronary heart disease by altering plasma lipoprotein concentrations, by increasing HDL cholesterol and decreasing LDL cholesterol, and thereby inhibiting progression of coronary artery
atherosclerosis
. Oral contraceptive can induce deterioration in glucose tolerance that has consistently been associated with insulin excess and insulin resistance. This situation can increase the coronary heart disease risk. New findings suggest that there may be independent cardioprotective effects of estrogen, such a direct inhibitory influence on thrombosis, vasospasm or atherogenesis, inhibiting atherosclerotic plaque formation in arterial walls.
...
PMID:[Sex hormones, glycolipid metabolism, and atherogenesis]. 756 60
Low-dose estrogen replacement therapy should be recommended to post-menopausal women, especially if they suffer from circulatory disorders, because it significantly reduces cardiovascular risk. Low-dose estrogens favourably affects lipid profile, without causing a significant increase of thrombotic risk:
atherosclerosis
is therefore prevented.
Estrogen
can augment coronary flow by the relaxation of vascular smooth-muscular cells. Finally, estrogen can improve left ventricle systolic and diastolic function, delaying the physiological aging process.
...
PMID:[Estrogens, left ventricular function and coronary circulation: what are the possibilities of therapeutic use?]. 764 87
Monokines, including tumor necrosis factor alpha (TNF-alpha), have been implicated in the pathogenesis of several pathologic processes, including
atherosclerosis
. Because estrogen has been found to offer a certain degree of protection against atherosclerotic progression, we examined the effect of estrogen on the expression of TNF-alpha mRNA in a monocyte-macrophage cell line, THP-1. Cells were exposed to 12-O-tetradecanoylphorbol 13-acetate (TPA, 50 ng/ml) for 48 or 96 h to induce differentiation. Some of the cells were treated with lipopolysaccharide (LPS, 10 micrograms/ml) in the last 3 h and/or
ethinyl estradiol
(estrogen, 10(-9) M) in the last 20 h. Total cellular RNA was isolated and cDNA synthesized and than coamplified using the polymerase chain reaction (PCR) in the presence of two sets (pairs) of 32P-labeled primers, one for TNF-alpha (product size 325 bp) and the second for the internal control, glyceraldehyde 3-phosphate dehydrogenase (G3PDH; 983 bp). The resultant PCR products were separated by agarose gel electrophoresis, and the ratios of radioactivity incorporated into TNF-alpha PCR products to G3PDH products were used to assess the relative changes in the levels of TNF-alpha mRNA abundance in response to various substances. Treatment with TPA for 48 h induced the expression of TNF-alpha mRNA. Treatment of these TPA-stimulated cells with estrogen caused a 62% decrease in TNF-alpha message abundance (p < 0.01). Similar results were obtained with cells stimulated with TPA for 96 h.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Estrogen modulates the expression of tumor necrosis factor alpha mRNA in phorbol ester-stimulated human monocytic THP-1 cells. 770 11
To evaluate the lipid and lipoprotein changes induced by a triphasic oral contraceptive (OC) containing
ethinyl estradiol
and gestodene, 25 healthy women from the Baltimore metropolitan area were enrolled in an open-label, noncomparative study. Serum lipids were measured prior to starting the OCs and again during the 3rd, 6th and 12th treatment cycles. Mean lipid concentrations in each treatment cycle were compared to baseline levels using the t test for paired samples. Small but statistically significant (P < or = .05) increases in the mean concentrations of total cholesterol, total triglycerides, total high density lipoprotein (HDL) cholesterol, HDL3 cholesterol, apolipoprotein A1 and apolipoprotein B were noted. Although the increases were statistically significant, the mean lipid concentrations were still within the normal range. The mean HDL2 and low density lipoprotein cholesterol concentrations were unchanged, as was the mean total cholesterol/HDL ratio. Healthy women taking a triphasic OC containing
ethinyl estradiol
and gestodene have minimal changes in lipids and should not be at increased risk of
atherosclerosis
due to OC-induced lipid alterations.
...
PMID:Lipoprotein alterations from a triphasic oral contraceptive containing ethinyl estradiol and gestodene. A 12-month trial. 780 86
Estrogen
use is associated with protection from cardiovascular disease in postmenopausal women. This benefit appears to be magnified among women with pre-existing heart disease. The possible bias of intrinsically better health in women using estrogen has not been ruled out in observational studies. Therefore, two double-blind randomized clinical trials are underway in postmenopausal women. One in women with coronary disease is known as HERS (Heart
Estrogen
-progestin Replacement Study) and another in predominantly healthy women is the WHI (Women's Health Initiative). Several mechanisms of estrogen mediated protection from cardiovascular disease have been identified including increased HDL, lower LDL, lower VLDL-cholesterol/triglyceride ratio, increased clearance of intermediate density lipoprotein (IDL) and LDL via an upregulated LDL receptor, diminished penetration and degradation of LDL in the arterial wall, an inhibition of LDL oxidation by various estrogens and a reversal of inappropriate acetylcholine (EDRF)-mediated vasoconstriction in arteriosclerotic vessels. The predominating mechanism is not known, but estrogen replacement therapy is both likely to be beneficial to female health, pending randomized trials, as well as a tool to understand mechanisms of prevention of coronary artery disease.
Atherosclerosis
1994 Oct
PMID:Effects of estrogens on lipoprotein metabolism and cardiovascular disease in women. 785 90
Monokines, such as interleukin-1, have been implicated in the pathogenesis of several pathologic processes, including the initiation and progression of
atherosclerosis
. Since estrogen has been identified as a modulator of
atherosclerosis
progression, we sought to examine the effect of estrogen on the inducible expression of interleukin-1 beta (IL-1 beta) and interleukin-1 alpha (IL-1 alpha) mRNA in the monocytic cell line, THP-1. Cells were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) (50 ng/ml) for 48 or 96 h to induce differentiation. Some cells were treated with lipopolysaccharide (LPS) (10 micrograms/ml) in the last 3 h and/or 10(-9) M
ethinyl estradiol
(estrogen) in the last 20 h. Total cellular RNA was isolated, and cDNA was synthesized and amplified using the polymerase chain reaction (PCR) using two sets (pairs) of 32P-labeled primers, one for IL-1 beta (product size 388 bp) and the second for the internal control, beta-actin (1126 bp), or to detect another cytokine mRNA, a set of primers for IL-1 alpha (product size 420 bp) and beta-actin. The PCR products were separated on a 3.0% agarose gel and the ratio of radioactivity incorporated into cytokine PCR products and beta-actin products was determined to assess the relative changes in the relative levels of cytokine to beta-actin mRNA abundance in response to various inducers. Treatment with TPA for 48 h induced expression of IL-1 beta mRNA, an effect that was enhanced two fold by LPS.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The inducible expression of THP-1 cell interleukin-1 mRNA: effects of estrogen on differential response to phorbol ester and lipopolysaccharide. 818 19
High concentrations of lipoprotein(a) [Lp(a)], an independent risk factor for
atherosclerosis
, cannot be managed by the usual lipid-lowering agents. It has been suggested that Lp(a) levels are related to female sex hormones.
Estrogen
replacement therapy makes the lipid profiles favorable for delaying
atherosclerosis
in postmenopausal women. The effects of the combination therapy of estrogen and progesterone on lipids are controversial. This study was designed to evaluate the effect of female sex hormones on the concentration of Lp(a) and to clarify the influence of progesterone on the effect of estrogen in postmenopausal women. Postmenopausal women (n = 184) were divided into four groups: control; 0.625 mg conjugated equine estrogen (CEE) plus 10 mg medroxyprogesterone acetate (MPA); 0.625 mg CEE plus 5 mg MPA; and 0.625 mg CEE only. Medication for 2 months lowered the concentrations of Lp(a) by 20% in all treated groups. The decrease was more pronounced in subjects with a relatively higher basal Lp(a) concentration.
Estrogen
replacement therapy raised the concentration of high-density lipoprotein cholesterol and decreased low-density lipoprotein cholesterol without changing total cholesterol. The combination therapy of estrogen and progesterone abolished the effect of estrogen on high-density lipoprotein cholesterol. Hormone replacement therapy lowered Lp(a) levels in postmenopausal women. The effect was prominent in subjects with high basal Lp(a) levels. This decrease may be one of the mechanisms of the cardioprotective effects of estrogen. The cardioprotective effect of estrogen cannot be applied to the combination therapy due to the adverse effect of progesterone on high-density lipoprotein cholesterol.
...
PMID:Effects of hormone replacement therapy on lipoprotein(a) and lipids in postmenopausal women. 830 20
The JCR:LA-cp rat exhibits an obese, insulin resistant, hyperlipidemic syndrome. Obese male rats, only, develop
atherosclerosis
and ischemic myocardial lesions. The obese males have a greater hyperinsulinemia, but the obese females have a much greater hypertriglyceridemia due to hypersecretion of very low density lipoprotein (VLDL). Obese rats of both sexes were surgically castrated at 6 weeks of age to study the influence of testosterone and estrogen secretion on the sexual dimorphism of metabolism and disease in this strain. Castration had no effect on body weight or food consumption up to 16 weeks of age. Castrated male rats had significantly improved glucose tolerance, but a doubled serum triglyceride concentration. Castrated female rats showed approximately halved triglyceride levels. The distribution of the triglyceride molecular species was altered in the castrated male rats to resemble that of the females in which there was no change with castration. The effects suggest that testosterone may inhibit hepatic triglyceride secretion and promotes insulin insensitivity.
Estrogen
appears to exacerbate hepatic hypersecretion of VLDL. Castration had no effect on myocardial lesion frequency in 9-month-old rats of either sex. This implies that estrogen does not exert a direct protective effect against cardiovascular disease in this animal model.
Atherosclerosis
1993 Apr
PMID:Effect of castration on hyperlipidemic, insulin resistant JCR:LA-corpulent rats. 831 56
Scintigraphic detection of atherosclerotic lesions using 111In-polyclonal IgG was studied. In Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for hypercholesterolemia with spontaneous
atherosclerosis
, aged WHHL rabbits incorporated more 111In-IgG into atherosclerotic lesions than young WHHL or control NZW rabbits. This result is in agreement with histological analysis. However, due to the low ratio of lesion-incorporated radioactivity to circulating radioactivity, in vivo gamma imaging of
atherosclerosis
with 111In-IgG scintigraphy was unsuccessful. Interventional agents, Probucol or vitamin E, used for 28 days to reduce the amount of autoantibodies produced against biological modified low-density lipoproteins did not produce differences in 111In-IgG incorporation into the aorta ex vivo.
Ethinylestradiol
, used for 28 days, exhibited similar incorporation with decreased serum cholesterol by 45%. Although
atherosclerosis
histology and lesion surfaces of WHHL rabbits are similar to those in adult humans, it is obvious that noninvasive gamma imaging with polyclonal 111In scintigraphy is not reliable for serial evaluation of the extent of
atherosclerosis
. Our results emphasize the need to develop pharmaceuticals to image
atherosclerosis
.
...
PMID:Evaluation of indium-111-polyclonal immunoglobulin G to quantitate atherosclerosis in Watanabe heritable hyperlipidemic rabbits with scintigraphy: effect of age and treatment with antioxidants or ethinylestradiol. 832 92
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