Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In autoimmune hyper- or dislipidemia secondary to a monoclonal antilipoprotein gammapathy, immunoglobulin-lipoprotein (Ig-Lp) complexes are found in the circulating blood. In order to determine their possible significance in common types of hyperlipidemia we compared the Ig-Lp content of sera from 98 healthy blood donors and 155 outpatients from a Lipid Clinic, including 91 cases of hypercholesterolemia (55 familial and 36 non-familial), 15 cases of hypertriglyceridemia, 20 cases of mixed hyperlipidemia and 29 miscellaneous cases. Detection of the Ig-Lp was performed by an ELISA technique with polyclonal affinity purified anti-LDL + HDL as capture antibodies and peroxidase-labeled anti-Ig antibodies specific for IgA, IgG, IgM heavy chains as indicators. Two cases of monoclonal gammapathy (one IgA K and one IgG L) with dislipidemia served as positive controls for the test. IgG, IgA and IgM Lp were found in the sera of the blood donors, in very small quantities when compared with the monoclonal gammapathy cases. All three types of Ig-Lp were also found in the different hyperlipidemic populations studied. When blood donors were compared to hyperlipidemic patients, no difference was observed for IgG Lp. A significant increase in IgM Lp was found in patients with familial hypercholesterolemia (P less than 0.01). An increase in IgA Lp was also found in hypercholesterolemia, familial or not (P less than 0.01), and in patients with corneal arcus (P less than 0.0001), ischaemic disease (P less than 0.01), tendon xanthomas (P less than 0.05) or xanthelasma (P less than 0.05). Furthermore, in a group of 18 paired parents from 9 different families, positive interparent correlations were found for IgM Lp (r = 0.78; P = 0.013) and IgG Lp (r = 0.69; P = 0.038). Therefore IgM Lp may be markers for subpopulations of familial hypercholesterolemia, and IgA Lp markers for the risk of atherosclerotic ischemic disease and deposition of lipids in the cornea. It may be (1) that natural clones of autoanti-lipoprotein antibodies are responsible for the minute quantities of Ig-Lp found in normal people; (2) that the marked development of one of these clones is the cause of autoimmune hyper- or dyslipidemia and xanthomatosis associated with monoclonal gammapathy; (3) that the limited development of a clone produces the Ig-Lp particles found in hypercholesterolemic patients; (4) that there are types of Ig-Lp particles (IgA Lp) that may be harmful for tissues independently of hypercholesterolemia.
Atherosclerosis 1988 Dec
PMID:Immunoglobulin-bound lipoproteins (Ig-Lp) as markers of familial hypercholesterolemia, xanthomatosis and atherosclerosis. 324 Mar 31

We have examined whether the toxic effects of homocysteine on cultured endothelial cells could result from the formation and action of hydrogen peroxide. In initial experiments with a cell-free system, micromolar amounts of copper were found to catalyze an oxygen-dependent oxidation of homocysteine. The molar ratio of homocysteine oxidized to oxygen consumed was approximately 4.0, which suggests that oxygen was reduced to water. The addition of catalase, however, decreased oxygen consumption by nearly one-half, which suggests that H2O2 was formed during the reaction. Confirming this hypothesis, H2O2 formation was detected using the horseradish peroxidase-dependent oxidation of fluorescent scopoletin. Ceruloplasmin was also found to catalyze oxidation of homocysteine and generation of H2O2 in molar amounts equivalent to copper sulfate. Finally, homocysteine oxidation was catalyzed by normal human serum in a concentration-dependent manner. Using cultured human and bovine endothelial cells, we found that homocysteine plus copper could lyse the cells in a dose-dependent manner, an effect that was completely prevented by catalase. Homocystine plus copper was not toxic to the cells. Specific injury to endothelial cells was seen only after 4 h of incubation with homocysteine plus copper. Confirming the biochemical studies, ceruloplasmin was also found to be equivalent to Cu++ in its ability to cause injury to endothelial cells in the presence of homocysteine. Since elevated levels of homocysteine have been implicated in premature development of atherosclerosis, these findings may be relevant to the mechanism of some types of chronic vascular injury.
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PMID:Endothelial cell injury due to copper-catalyzed hydrogen peroxide generation from homocysteine. 351 79

The distribution of apolipoprotein E (apo E) immunoreactive substances (IRS) in atherosclerotic lesions and lesion-free areas of the aorta and coronary arteries obtained from 17 autopsied cases was studied using a specific anti-apo E serum and the unlabeled peroxidase-antiperoxidase (PAP) method. In fatty streak lesions of the aorta, many cells containing apo E-IRS were found in the deeper layer of the intima and diffuse staining of apo E in the extracellular spaces was also noted. In more advanced lesions apo E-positive cells could not be found. Immunohistochemical findings of coronary arteries differed distinctly from those of the aorta in that the apo-E-positive cells were absent in the deeper layer of the intima. The endothelial cells of coronary arteries, but not those of the aorta, showed positive staining for apo E.
Atherosclerosis 1986 Apr
PMID:Immunohistochemical localization of apolipoprotein E in atherosclerotic lesions of the aorta and coronary arteries. 351 33

In order to assess the possible utility of lectin binding to identify the cellular components of fixed arterial lesions we studied lectin binding in experimental rabbit and monkey vessels, as well as in human atherosclerotic arteries obtained at surgery. The avidin-biotin-peroxidase technique was used to localize the binding of the following biotinylated lectins: Concanavalin A (Con A), Dolicho biflorus agglutinin (DBA), soybean agglutinin (SBA), peanut agglutinin (PNA), Phaseolus vulgaris agglutinin (PHA), Ricinus communis agglutinin (RCA), wheat germ agglutinin (WGA), and Ulex europaeus agglutinin (UEA). PHA demonstrated specific cytoplasmic staining of macrophages in rabbit, monkey, and human tissues and differentiated macrophages from other cell types in atherosclerotic lesions. When morphometric comparisons were made between lesion PHA staining and another macrophage marker, acid lipase, very similar results were obtained. Con A, RCA, and WGA stained macrophages intensely and differentiated them from other cell types in normal reticuloendothelial tissues and lesions, but also stained smooth muscle cells and endothelial cells when these cells developed lipid vacuoles. UEA stained the endothelium of vasa vasorum consistently in human arteries, but staining of artery lumen endothelium was variable. Endothelial cells of rabbit or monkey vessels did not stain with UEA. DBA, PNA, and SBA did not consistently stain any cellular structures in arteries. PHA was found to be an excellent marker to differentiate and quantify macrophages in glutaraldehyde or formalin-fixed, paraffin-embedded experimental and human atherosclerotic lesions. Con A, RCA and WGA merit further detailed study in conjunction with other histochemical tests as possible markers of functional changes in arterial cells during lesion development.
Atherosclerosis 1986 Sep
PMID:Lectin binding to distinguish cell types in fixed atherosclerotic arteries. 353 93

Samples from 34 patients were studied both histologically and immunocytochemically by the indirect biotin-avidin peroxidase technique to analyse the distribution of the extracellular matrix components (type IV collagen, fibronectin, types I and III collagens) in dissection of the aorta. Most showed defects in type IV collagen around medial smooth muscle cells. Defects in smooth muscle cell basement membrane were found throughout the media in cystic medial degeneration and in medionecrosis, whereas in atherosclerosis such unlabelled areas were found only above advanced atherosclerotic plaques. In aortitis other defects in the smooth muscle cell basement membrane were found in areas of inflammatory infiltrates. In all of these conditions similar defects in fibronectin expression were also found. No defects in the expression of interstitial collagens type I and III were seen in the dissecting aortas. Moreover, cystic medial degeneration, medionecrosis, and atherosclerosis were characterised by intense staining of these interstitial matrix components. In the pathogenesis of the aortic dissection local changes in the basement membranes of the medial layer may be important.
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PMID:Histological pattern and changes in extracellular matrix in aortic dissections. 353 14

A histopathological and histoimmunological comparison was performed on 143 fragments on coronary arteries taken from 43 patients who died of ischemic heart disease and from 20 patients who died of other diseases. The immunological study research of Ig (A, G, M) and C3 fraction of complement in the 3 coronary layers was done by the immuno-peroxidase technique. The fixation was essentially observed in fibromyocytes. A good correlation existed between atherosclerosis lesions and fixation of Ig and C3 fraction of complement in both the media and the intima. On the other hand, this correlation was not observed in the adventitia. Accumulation of immunoglobulins and of the C3 fraction of complement in atherosclerosis seemed specific and proportional to the degree of arterial well lesion. The significance and the role of this accumulation remains to be studied. It may be hypothesized that Ig and complement fixation on fibromyocyte cell receptors or on the fibrous tissue fundamental substance is followed by the formation of antigen-antibody complexes, which act as foreign bodies which are either responsible for (or a reflection) of the onset of lesions or, at least, of their increasing severity or their persistence.
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PMID:[Presence of immunoglobulins and complement in the walls of the coronary arteries in atherosclerosis]. 353 28

Aortas, coronary and carotid arteries from 31 patients who died of myocardial or cerebral infarction were examined by direct immunoenzymatic tests (using peroxidase-labelled anti human IgG sheep Fab or anti human complement sheep IgG) and compared to those of 9 patients who died of non atherosclerotic diseases. Immunoglobulins and complement bound to all atherosclerotic lesions, all elastic fiber alterations, all lipid infiltration in patients who died of atherosclerosis, as well as in patients who died of various other causes. Binding was generally more intensive in patients who died of atherosclerosis and in arteries irrigating infarcted areas. These data are discussed.
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PMID:[Possible intervention of immune mechanisms in the genesis and course of human atherosclerosis]. 389 42

Endothelia lining the 2 surfaces (arterial and ventricular) of the posterior cusp of aortic valves from normocholesterolemic, New Zealand white rabbits were found to display pleomorphic surface features characterized by differences in cellular shape and orientation to the direction of blood flow, microappendage populations (microvilli and blebs), nuclear contours and the surface reactions of cationic dyes (RR, AB) and peroxidase-conjugated lectins (Con A, Limulin, WGA). With the aid of SEM and TEM, the cells lining the arterial surfaces appeared relatively smooth and flattened with a moderate to heavy reaction of the carbohydrate cell coat at the blood interface. By contrast, the contours of the endothelia lining the ventricular surfaces were noticeably raised with numerous plasmalemmal microappendages and only a moderate dye/lectin reaction. Observations of similar endothelial populations from diet-induced, hypercholesterolemic rabbits (500 mg/dl) revealed a variety of dramatic changes in the cells lining the arterial surfaces of the valvular cusps. No severe changes were observed in the endothelia of the ventricular surfaces. Such findings are suggestive further of the importance of the interaction between the environment and the endothelial cell coat as influencing factors in the onset of intramural lipid infiltration.
Atherosclerosis 1985 Mar
PMID:Surface responses of aortic valve endothelia from diet-induced, hypercholesterolemic rabbits. 399 84

Cardiac rupture occurs in 10 per cent of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Twenty randomly selected patients with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the two groups (5.7 +/- 5.8 days for patients with rupture versus 4.2 +/- 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the two groups, with 55 per cent of the patients with cardiac rupture having single-vessel disease and 70 per cent of the patients without cardiac rupture having disease in three vessels. Additionally, the incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in ten high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P less than 0.01) greater in hearts associated with cardiac rupture (29.5 +/- 4 per cent) than in control hearts (11.7 +/- 3.1 per cent). It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.
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PMID:Association of eosinophils with cardiac rupture. 399 34

Hepatocatalase peroxidase, an active peroxidase-oxidase subunit isolated from beef-liver catalase, prevents cholesterol deposition and aortic atherosclerosis in cholesterol-fed rabbits and has no apparent toxicity or undesirable de effects. No allergic or immunological reactions have been observed. The participation of this enzymatic subunit in homeostatic control mechanisms and its potential pharmacological value in the control of human atherosclerosis are suggested.
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PMID:Prevention of induced atherosclerosis by peroxidase. 601 53


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