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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methylated DNA-binding protein (MDBP), a sequence-specific DNA-binding protein, was found to recognize more than 30 sites within an allele of the human apolipoprotein(a) gene. High plasma levels of apolipoprotein(a), a risk factor for atherosclerosis, have been correlated with genetically inherited lower-molecular-mass isoforms of this protein. MDBP might help down modulate the expression of the apolipoprotein(a) gene in a manner dependent on the length of a given allele of the gene and the number of MDBP sites in it.
Mol Cell Biol 1990 Sep
PMID:Highly repeated sites in the apolipoprotein(a) gene recognized by methylated DNA-binding protein, a sequence-specific DNA-binding protein. 238 31

We have examined foam cell accumulation in abdominal and thoracic aortic segments of swine with experimentally induced atherosclerosis. Young (less than 1-year-old) male swine were divided into four groups that were fed control, lard (20%), lard (20%) plus cholesterol (1%), and regression (3 months cholesterol-lard followed by 3 months control) diets for 6 months. Aortas were removed from animals and enzymatically dissociated. Foam cells were detected by specifically staining their cholesteryl ester inclusions with the fluorescent dye filipin. Flow cytometry was used to quantify the number of foam cells in each aortic cell suspension. Cholesterol-lard feeding increased serum cholesterol levels 6-fold and induced a substantial increase in both abdominal and thoracic foam cell densities. Lesion development in cholesterol-lard-fed animals, as assessed by macroscopic evaluation of aortas, correlated with foam cell accumulation as determined by flow cytometry. Accumulation of foam cells was extremely variable from animal to animal and did correlate significantly with serum cholesterol but not with serum triglyceride levels. Interestingly, although serum cholesterol levels increased 1.5-fold in swine fed the lard diet, foam cells did not increase significantly as compared to control animals. Animals placed on a control diet following 3 months of the cholesterol-lard diet showed a trend toward lower foam cell densities as compared to animals fed the cholesterol-lard diet for the entire 6 months. Flow cytometric analysis of filipin-stained aortic foam cells provides a new means to evaluate atherosclerotic lesion development.
Exp Mol Pathol 1987 Feb
PMID:Flow cytometric quantification of cholesteryl ester-containing "foam" cells. II. Analysis of aortas from cholesterol-fed swine. 243 51

A primary culture of cells derived from uninvolved and atherosclerotic intima of human aorta was used to elucidate the role of cyclic nucleotides in atherogenesis. The cells cultured from fatty streaks and atherosclerotic plaques had a 2- to 8-fold lower cyclic AMP level and a 1.5- to 2-fold higher level of cyclic GMP compared with those of a grossly normal intima. Medial cells cultured from nonlesioned and atherosclerotic aortic segments showed no differences in the cyclic nucleotide concentrations. Reduction of the intracellular cyclic AMP with 2'-deoxyadenosine or a cyclic GMP elevation with its dibutyryl derivative, or liposomes containing cyclic GMP stimulated the uptake of [3H]thymidine and protein synthesis in the cells cultured from unaffected intima. On the contrary, a rise of the intracellular cyclic AMP caused by adenylate cyclase activators, a phosphodiesterase inhibitor, dibutyryl cyclic AMP, and liposomes containing cyclic AMP inhibited cell proliferation and protein synthesis. Elevation of the intracellular cyclic AMP stimulated the hydrolysis of lipids which led to reduction of lipid levels in the cells cultured from atherosclerotic lesions. The results of this study corroborate the existence of a relationship between the alterations of intracellular cyclic nucleotide levels and the metabolic disorders occurring in atherosclerosis.
Exp Mol Pathol 1987 Dec
PMID:Cyclic nucleotides and atherosclerosis: studies in primary culture of human aortic cells. 244

This is a review of the utilization of cynomolgus monkeys (Macaca fascicularis) in atherosclerosis research. Naturally occurring and experimentally induced atherosclerosis progression and regression studies are described. This species has been utilized as an animal model to study the effects of immunologic injury, aging, exercise, and drug intervention on atherosclerotic lesions. Cynomolgus macaque atherosclerosis induced by feeding cholesterol is a good model of human atherosclerosis because of similar gender-related differences in susceptibility to coronary artery atherosclerosis, a relatively high incidence of myocardial infarction, and characterized psychosocial factors that influence the development of atherosclerosis.
Exp Mol Pathol 1989 Feb
PMID:Atherosclerosis research in cynomolgus monkeys (Macaca fascicularis). 264 42

A technique is described which provides morphologic and quantitative data on the amount of oil red O (ORO) staining in thoracic aortas of rats fed a high cholesterol diet. Samples are stained with ORO, the dye is extracted, and the concentration of ORO in the extract is measured colorimetrically. Wistar rats fed ad libitum either standard chow (control group: n = 15) or chow supplemented with 4% cholesterol, 1% cholic acid, and 0.5% thiouracil (CCT group: n = 23) were maintained on these diets for 1, 3, 6, 9, or 12 months. Plasma cholesterol levels averaged overall 87 and 737 mg/dl for the control and CCT groups, respectively. Animals were killed under anesthesia by perfusion fixation with formalin or glutaraldehyde, and samples of thoracic aorta were stained with ORO. After microscopic study en face and measurement of surface area, the ORO was extracted in chloroform-methanol (2:1). Concentrations of ORO (microM) were determined from a standard curve and expressed as microM/mm2 of aorta. Aortas of CCT animals showed progressive diet- and time-dependent increases in the amount of ORO staining compared to controls. We conclude that this method yields reliable quantitative data applicable to studying atherosclerosis in small animals.
Exp Mol Pathol 1989 Aug
PMID:Quantitation of oil red O staining of the aorta in hypercholesterolemic rats. 276 15

Normal arterial foci which take up Evans blue dye (EBD) in vivo are believed to represent atherosclerosis-prone, hemodynamically stressed foci compared to areas which exclude dye. We have used the rabbit EBD model to examine focal aortic hydrolases of blue areas versus white areas, and we report herein significant focal variations of hydrolase activities. Enzymes measured included neutral alpha-glucosidase, N-acetyl-beta-glucosaminidase, alpha-mannosidase, acid alpha-glucosidase, beta-galactosidase, beta-glucuronidase, cathepsin C, and acid cholesteryl esterase (ACE); specific activities were expressed on the basis of tissue DNA. In correlative areas of EBD uptake in normal rabbit aortic arch, ACE activity averaged 17% higher and cathepsin C activity averaged 37% lower than activities of areas free of EBD in the descending thoracic aorta (P less than 0.02). None of the glycosidases studied differed significantly between blue and white aortic areas. These findings indicate that discrete, intrinsic differences of hydrolytic enzyme activities exist in the normal rabbit aorta in areas delineated by in vivo EBD uptake, areas recognized as lesion-prone vs lesion-resistant.
Exp Mol Pathol 1989 Aug
PMID:Intrinsic focal variations of rabbit aortic hydrolase activities. 276 19

Arteriovenous fistulae between the external jugular vein and the common carotid artery were surgically fashioned in eight sheep. The altered hemodynamics produced morphological changes similar to those observed in human atherosclerosis. The elastica is a major mural component and undergoes considerable structural variation during lesion development. The most significant biochemical changes in the elastin occur in the experimental vein region. These include a quantitative loss particularly in the midregion of the vein and a decrease in the concentration of up to 20% of the crosslinks (desmosine and isodesmosine). There is an increase in the cholesterol content of the elastin purified from both experimental artery and vein. The bound phospholipid was higher in the experimental artery and in the dilated experimental vein. There was a significant time-dependent loss of elastin in the stressed venous tissue.
Exp Mol Pathol 1989 Oct
PMID:The biochemical composition of hemodynamically stressed vascular tissue: the insoluble elastin of experimental arteriovenous fistulae. 280 66

During the early stages of atherogenesis, as well as during in vitro cultivation, smooth muscle cells modulate from a contractile to a synthetic phenotype. This process includes the loss of myofilaments and the formation of an extensive rough endoplasmic reticulum and a large Golgi complex; it leads to decreased contractility and the commencement of cell growth and secretion of extracellular matrix components. In this paper, the effects of nicotine on adult rat arterial smooth muscle cells cultivated in vitro were studied by transmission electron microscopy and 3H-thymidine autoradiography. The results show that the drug speeded the initial rate of transition of the cells from contractile to synthetic phenotype in primary culture. Further, it stimulated the initiation of DNA synthesis in growth-arrested secondary cultures. Its effect was independent of other mitogens and additive to that of serum. The influences of nicotine, both on the modulation of the smooth muscle phenotype and the initiation of DNA synthesis, occurred at concentrations lower than those obtained in the blood after smoking and could contribute to the role of smoking as a risk factor for atherosclerosis.
Virchows Arch B Cell Pathol Incl Mol Pathol 1986
PMID:Effects of nicotine on phenotypic modulation and initiation of DNA synthesis in cultured arterial smooth muscle cells. 288 92

Cardiac enlargement and dysfunction are common in patients with acromegaly. Whether these changes are a direct consequence of growth hormone excess is obscured by the high frequency of hypertension, diabetes mellitus, or atherosclerosis in acromegalic patients. In this study, the effects of chronic elevations of growth hormone (GH) upon the heart were studied in rats with GH-producing tumours implanted subcutaneously for 4 weeks. Geometric measurements and histology were employed to detect the presence of cardiac changes. Increased mass was observed in the tumour-bearing animals. When compared with controls, in tumour-bearing rats there were significantly greater (P less than 0.05) right (0.17 +/- 0.03 v. 0.13 +/- 0.01 g) and left (0.62 +/- 0.05 v. 0.50 +/- 0.04 g) ventricular weights, external cardiac dimensions, and myocardial fibre diameters (9.4 +/- 0.6 v. 8.3 +/- 0.4 micron). However, these increases were linearly-related to increased body mass in the tumour-bearing group so that the ratios of ventricular weights to body weight were similar in both groups. Furthermore, no pathologic changes such as myocardial fibrosis or asymmetric septal hypertrophy were present in the tumour-bearing rats. Thus, under the conditions of this study, growth hormone excess induced cardiac growth, which appeared to represent a manifestation of generalized body growth rather than a distinct pathologic process.
J Mol Cell Cardiol 1985 Aug
PMID:Cardiac morphology in rats with growth hormone-producing tumours. 293 34

Apolipoprotein B (apoB) is the major protein component of low-density and very-low-density lipoproteins. We have recently isolated nonoverlapping cDNA clones for apoB and confirmed their identity by sequence comparisons. We now report the mapping of the human apoB gene (APOB) to the p23-p24 region of chromosome 2 by examination of human-mouse somatic cell hybrids and by in situ hybridization to human chromosomes. Thus, APOB is unlinked to members of the dispersed gene family encoding other apolipoprotein species or to the gene encoding the low-density lipoprotein receptor. Hybridization analysis with genomic DNA and liver and intestinal mRNA suggests that APOB encodes both the high-molecular-weight form of apoB (apoB100) incorporated into very-low-density lipoproteins in liver and the lower-molecular-weight form (apoB48) incorporated into chylomicrons in intestine. Restriction fragment length polymorphisms of APOB have been identified and should prove useful in examining the possibility that genetic variations of APOB are involved in dyslipoproteinemias and atherosclerosis.
Somat Cell Mol Genet 1986 May
PMID:Human apolipoprotein B: chromosomal mapping and DNA polymorphisms of hepatic and intestinal species. 301 97


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