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)

The sensitive and reliable dinitrophenyl (DNP) hapten sandwich staining (DHSS) procedure (B. Jasani et al., Virchows Arch (Pathol. Anat.), 406 (1985) 441-448) was used to study the distribution of immunoperoxidase staining seen with antibodies to seven protein markers in post-mortem heart tissue. This was obtained from 12 cases with macroscopic myocardial infarction and 17 cases without myocardial infarction (10 with and 7 without significant coronary artery atherosclerosis). The immunostaining patterns were compared with the appearances seen in adjacent sections stained by the routine haematoxylin and eosin (H & E) and phosphotungstic acid haematoxylin (PTAH) methods and a method previously recommended for the detection of early myocardial infarction, the haematoxylin basic fuchsin picric acid (HBFP) stain. Loss of immunostaining with an antibody to myoglobin was found to be a reliable and more objective marker of both early and established myocardial infarction compared with the histological stains. Antibodies to myosin, caeruloplasmin, C-reactive protein and pre-albumin gave similar but less reliable results, whilst those to complement factor C3b and alpha-1 anti-trypsin gave the least reliable results for early myocardial ischaemic/hypoxic damage. The immunocytochemical results are considered sufficiently encouraging to extend the work to a large number of sudden death cases in order to establish a new, more reliable approach to the detection of histologically latent ischaemic/hypoxic damage in the myocardium.
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PMID:Immunocytochemical diagnosis of early myocardial ischaemic/hypoxic damage. 264 26

Subendothelial cells (SEC) were obtained from the inner intimal layer of adult human aorta by collagenase treatment. SEC were identified in primary culture either as smooth muscle cells by staining with FITC-labeled antisera against human smooth muscle myosin or as macrophages, foam cells and contaminating endothelial cells by their uptake of malondialdehyde treated low density lipoproteins labeled with fluorescent dye 3,3'-dioctadecylindocarbocyanine. Between 1 and 5 days in culture, along with smooth muscle cells (SMC, 38-82%), endothelial cells (0-9%), macrophages and foam cells (2-32%), one more type of cell was found. This cell type resembled SMC in size and shape, but was not stained by antisera to SMC myosin. By ultrastructural criteria these cells were characterized as modulated SMC for they contained prominent rough endoplastic reticulum and Golgi complex together with basement membrane and a large number of plasmalemmal vesicles. Like SMC they reacted with phalloidin and were stained by anti-vimentin but not by anti-desmin monoclonal antibodies. The proportion of such cells varied from 5 to 33% of total cell number and increased in parallel to macrophages and foam cells in vessels with well developed atherosclerotic lesions. We conclude that the applied technique may be used for identification of cultured vascular cells including modulated SMC.
Atherosclerosis 1988 May
PMID:Identification of intimal subendothelial cells from human aorta in primary culture. 313 80

The phenotype of smooth muscle cells (SMCs) in the aortic media of 7 human fetuses (14-20 weeks of gestation) was examined with transmission electron microscopy, immunofluorescence microscopy, and gel electrophoresis of the cytoskeletal and cytocontractile proteins. Ultrastructurally, virtually all medial cells were identified as SMCs having a poorly differentiated phenotype with a cytoplasm rich in rough endoplasmic reticulum and organelles, and with only a few myofilaments. All medial cells stained intensely with antibodies to vimentin, but only in a 20-week-old fetus could we find a few SMCs staining with antibodies to desmin. Nor was desmin detectable with SDS gel electrophoresis followed by immunoblotting, while clear bands corresponding to vimentin, myosin, and actin were present. In isoelectric focusing and two-dimensional gel electrophoresis beta-actin was the most prominent of the 3 actin isoforms in all cases. The present results show that SMCs in the media of fetal human aorta have a poorly differentiated phenotype, which morphologically and biochemically resembles that previously described in the aorta of fetal and newborn rat, in the arterial intima after endothelial injury, in atherosclerotic lesions, and after spontaneous modulation of medial SMCs in culture.
Atherosclerosis 1988 Nov
PMID:Characterization of the phenotype of smooth muscle cells in human fetal aorta on the basis of ultrastructure, immunofluorescence, and the composition of cytoskeletal and cytocontractile proteins. 321 79

The authors probed the vascular endothelial cell cytoskeleton in strains of pigeons that are atherosclerosis-susceptible and disease-resistant, namely, the White Carneau and Show Racer pigeons. Endothelial cell actin and myosin were localized with the use of affinity-purified antibodies in conjunction with indirect immunofluorescence microscopy. The endothelial cell cytoskeleton was characterized in a site-specific and time-dependent manner by examination of arterial segments from each strain of pigeons. Anti-actin and anti-myosin fluorescence staining patterns of endothelial cells lining the ascending aorta, aortic arch, and thoracic aorta from the White Carneau and Show Racer pigeons sacrificed at 1 and 12 months of age were compared and analyzed. In the Show Racer, irrespective of arterial site or chronologic age, endothelial cell cytoskeletal organization is similar. Actin and myosin fluorescence is brightest at the cortex, where endothelial cells meet their neighbors. There is also an amorphous (diffuse) fluorescence throughout the cytoplasm. In addition to the diffuse and cortical cytoskeletal fluorescence in the endothelial cells of the Show Racers, the White Carneau also possess a unique cytoskeletal array of linear fluorescence, ie, the endothelial cell ridge. At 1 month of age, anti-actin staining of endothelial cell ridges averages 28.5 mu in length in the ascending aorta, 28.0 mu in the aortic arch, and 40.0 mu in the thoracic aorta. At the same time, anti-myosin fluorescence extends past both ends of the anti-actin-stained endothelial cell ridge fluorescence. In the ascending aorta, anti-myosin labeling of endothelial cell ridges is 3.5 times longer than anti-actin staining. This staining is absent in the aortic arch, whereas the thoracic aorta possesses endothelial cell ridges that extend over the entire length of the vessel segment. At 12 months of age, actin-stained endothelial cell ridges increase 1.6- and 1.4-fold in the ascending aorta and aortic arch, respectively. The thoracic aorta possesses endothelial cell ridges that cover its entire length. At 12 months of age, the length of myosin-stained endothelial cell ridges does not increase in the ascending or thoracic aorta. In contrast, the aortic arch expresses endothelial cell ridges that exceed 150 mu in length. It is proposed that the endothelial cell ridge assembles from cytoskeletal components as a focal endothelial cell response to injury, perhaps promoting endothelial cell adhesion to the underlying basal lamina through a transmembrane linkage.
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PMID:Age-related and site-specific adaptation of the arterial endothelial cytoskeleton during atherogenesis. 334 60

The effect of macrophages on rabbit vascular smooth muscle phenotype and proliferative ability was examined using ultrastructural morphometry. The volume fraction of myofilaments (Vv myo) in smooth muscle cells (SMC) from 9-week-old rabbit aorta in vivo was 39.5 +/- 1.2%. After seeding the enzymatically isolated SMC at 4 X 10(5) cells/ml in primary culture, the Vv myo was 38.9 +/- 1.2% on day 3 dropping to 29.9 +/- 2.0% by day 5. On day 6 the Vv myo was 29.2 +/- 1.8%, and the cells began to proliferate. Confluency was reached after less than 24 h proliferation and the Vv myo rose abruptly on day 7 to 36.9 +/- 1.9%. When the SMC were co-cultured with macrophages, the Vv myo fell to 31.2 +/- 0.9% on day 3 and to 25.9 +/- 0.5% on day 5 at which time cells commenced proliferation. Confluency occurred on day 6 but the SMC Vv myo did not rise throughout the rest of the culture period (27.4 +/- 1.8% and 26.9 +/- 1.3% on days 7 and 9, respectively) and the cells, unlike the controls, continued to proliferate, becoming multi-layered. Early phenotypic modulation in sparsely seeded SMC (8 X 10(4) cells/ml) co-cultured with macrophages was also found using fluorescent labelled antibodies to smooth muscle myosin. Measurement of proliferation by cell counts (and tritiated thymidine autoradiography) showed that macrophages stimulated SMC in primary culture to proliferate at a significantly greater rate than control cells grown alone in 5% whole blood serum (WBS). Proliferation of subcultured SMC co-cultured with macrophages was also stimulated.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1988 May
PMID:Vascular smooth muscle phenotype and growth behaviour can be influenced by macrophages in vitro. 337 79

35 autopsies--aged 30 to 75 years--were investigated in order to establish trends of collagen localization in various types of arteries depending on age, arterial size and degree of atherosclerosis. Cryostat sections stained with highly specific antibodies to human types I, III, IV or V collagen, or with the antiserum to smooth muscle myosin were examined by the indirect immunofluorescence technique. Localization of type III collagen was very similar to that of type I. Fibrous structures of both type I and type III were then major constituents of the intima, media and adventitia. Sparse fibrils of type I and type III collagens were revealed in the subendothelium of unaffected intima. They gradually became abundant in the deeper intimal layers contrasting with loose fibrillar formations of the media. The content of interstitial collagens was significantly increased in the subendothelium of local intimal thickenings and in a thickened intima of the aged. This fact, considering the thrombogenicity of interstitial collagens, may be relevant to the atherogenesis through the "response-to-injury" mechanism. Type IV and type V collagens are localized to the endothelial basement membrane and basement membranes of smooth muscle cells of the intima and media. Diffusely distributed type V collagen was also observed in the intercellular space of the intima. In lipid streaks, parallel layers of condensed interstitial collagens separated groups of cells and extracellular lipid depositions. In fibrous plaques, types I and III became prevalent structural elements and their densely packed fibers occupied whole regions devoid of any type IV and type V collagen. Heavily thickened type IV collagen structures surrounding individual smooth muscle cells were found in fibrous plaques, but never, in unaffected intima.
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PMID:Distribution of type I, III, IV and V collagen in normal and atherosclerotic human arterial wall: immunomorphological characteristics. 390 43

Although the endothelial cell (EC) cytoskeleton has been studied both in vitro and in vivo, little is known about its role in endothelial integrity. We have previously suggested that specific EC microfilament (MF) structure, which we have termed the "dense peripheral band (DPB)," may play a major role in this process. We have extended our studies to characterize this structure in pig aortic ECs in vitro. During the growth of EC cultures, the DPB appears only when the cultures have attained confluency. Using double fluorescent labeling, we found that alpha-actinin, myosin, and tropomyosin colocalized with the F-actin making up the DPB. Occasional microtubules were present in this region, although there was no preferred association between microtubules and the DPB. Colocalization studies revealed vinculin plaques at the cell-cell interface. Thin MFs extended from the DPB into the cytoplasmic side of these plaques. The DPB was completely disrupted by low dose cytochalasin B within 30 minutes, whereas many central MF bundles were still present at 24 hours. The results of this study suggest that the DPB is a distinct structure in the confluent EC monolayer and is closely associated with the ability of ECs to form and maintain the EC monolayer. The disruption of the DPB as an important initial event in the pathogenesis of vascular diseases such as atherosclerosis is discussed.
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PMID:Endothelial cell monolayer integrity. I. Characterization of dense peripheral band of microfilaments. 395 75

Diabetes mellitus causes congestive heart failure in humans, independent of atherosclerosis. The present study extends previous work on the reversibility, with insulin, of the alterations in myocardial function and contractile protein biochemistry observed in diabetic rats. The response of these alterations to different fixed doses of insulin was explored. Diabetic rats were given 0, 0.5, 1, 1.5, 2, or 2.5 U of insulin daily for 6 wk. Papillary muscle function, actomyosin ATPase, and myosin isoenzyme distribution showed progressive normalization with increasing insulin dose as blood glucose concentration returned to normal. Thus insulin therapy in diabetic rats on a normal diet produces continuous improvement in cardiac function and biochemistry as euglycemia is approached. This study also suggests that mild diabetes results in qualitatively identical, although quantitatively less pronounced, myocardial changes compared with those observed in severely diabetic rats.
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PMID:Diabetic cardiomyopathy in rats: mechanical and biochemical response to different insulin doses. 623 41

Aortic intima-medias of normal and cholesterol-fed rabbits were studied with EM and cells were isolated by enzyme digestion. The composition of cytoskeletal and cytocontractile proteins was determined with SDS-PAGE and the primary growth and thymidine incorporation rates were assessed after seeding the cells into tissue culture flasks. Ultrastructurally, the SMCs in the thickened atherosclerotic intima differed from the contractile medial SMCs in containing lipid vacuoles, enlarged endoplasmic reticulum and a reduced number of myofilaments, thus showing characteristics of dedifferentiated SMCs. In SDS-PAGE, freshly isolated cells from the atherosclerotic intima-medias had a lower content of myosin and actin, and a higher proportion of vimentin and desmin than SMCs from normal aortas. Enzyme-isolated SMCs from normal aortas did not start to grow and incorporate radioactive thymidine until 5-6 days after seeding, whereas those from atherosclerotic aortas did so within 2 days. After a week in culture, SMCs from both sources resembled each other, and had decreased contents of myosin and actin, and increased concentrations of vimentin in comparison to freshly isolated normal SMCs. The present results indicate (a) that morphological dedifferentiation of SMCs in aortic lesions of cholesterol-fed rabbits is associated with an increased proportion of the proteins of the intermediate filaments and a decrease in those of the thin and thick myofilaments as determined with SDS-PAGE, and (b) that similar changes take place when normal SMCs are cultured in vitro. The results also suggest (c) that enzyme-isolated atherosclerotic SMCs proliferate in a primary culture without the lag period that normal SMCs apparently require for dedifferentiation.
Atherosclerosis 1984 Jul
PMID:Growth properties and composition of cytoskeletal and cytocontractile proteins in aortic cells isolated and cultured from normal and atherosclerotic rabbits. 646 13

Mapping the distribution of an immature smooth muscle cell (SMC) subpopulation in large- and small-sized arterial vessels was carried out in normocholesterolemic rabbits and compared with the mapping atherosclerotic lesions in endogenously (Watanabe heritable hyperlipemic, WHHL) and exogenously derived (cholesterol-fed, CT) hypercholesterolemic rabbits. This cell subset is identified by a specific myosin isoform content and displays an intermediate degree of differentiation between fetal- and adult-type SMC. Monoclonal anti-myosin antibodies, immunofluorescence procedures, and different arterial segments of a rabbit vessel tree, i.e. from aorta to dental pulp (common carotid, external carotid, lingual, facial, maxillary, inferior alveolar arteries, and dental branches of alveolar arteries) were studied. WHHL of different ages (3 to 12 months), and two different concentrations of CT (2% and 0.2%) in the diet for 3 and 12 months, respectively, were used. The results of the present study indicate that: (1) using a diet with a higher percentage of CT (rabbits fed 2% CT-diet for 3 months) there is maximum expansion of atherosclerotic lesions from the aorta up to the maxillary artery; (2) localization of atherosclerotic lesions with a lower CT content in the diet is dependent on the duration of feeding and may involve the aorta up to the external carotid artery; (3) the development of the atherosclerotic lesion in hypercholesterolemic rabbit is strictly related to the appearance of an intermediate SMC subtype; (4) atherosclerotic lesions occur only in those arterial sites which, in corresponding normocholesterolemic rabbit, contain intermediate-type SMC; and (5) no differences can be found in the distribution of SMC subpopulations present in the lesions from WHHL, CT-fed animals, or at various arterial levels, whereas some discrepancies can be shown in aortic atherogenesis.
Atherosclerosis 1995 Jul
PMID:Correlation between the presence of an immature smooth muscle cell population in tunica media and the development of atherosclerotic lesion. A study on different-sized rabbit arteries from cholesterol-fed and Watanabe heritable hyperlipemic rabbits. 748 35


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