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At least 19 recordsLinked to original sources
PubMed1974

Lysosomes of the arterial wall. IV. Cytochemical localization of acid phosphatase and catalase in smooth muscle cells and foam cells from rabbit atheromatous aorta.

Cytochemical methods for acid phosphatase and catalase were applied to atheromatous aortas from cholesterol-fed rabbits. Whole tissue, partially digested aortic slices and isolated cells were used for the study. Present in the atheromatous lesions were smooth muscle cells in all stages of foamy transformation, from virtually normal appearing smooth muscle cells to severely altered cells with pronounced lipid accumulation. The results with the acid phosphatase method show that lysosomes increase both in size and in number as the smooth muscle cells become foam cells. In normal appearing smooth muscle cells, acid phosphatase reaction product was found in stacked cisternae of the Golgi apparatus and in small vesicles located in the Golgi region and distributed throughout the cytoplasm. In foam cells, reaction product was found in membrane-limited vacuoles of varying size which typically contained membranous debris or myelin-like figures together with massive lipid deposits. No reaction was seen in "free" cytoplasmic lipid droplets lacking a surrounding membrane. These results confirm and extend previous biochemical findings indicating that, in the cholesterol-fed rabbit, the change from normal smooth muscle cell to foam cell is accompanied by marked physical and chemical changes of the lysosomes, including their progressive overloading with cholesteryl ester. Small diaminobenzidine-positive particles were present in normal smooth muscle cells and in those at all stages of foamy transformation. These particles were more frequent in foam cells, in agreement with the marked increase in catalase activity detected biochemically in these cells.

Acid Phosphatase↗
PubMedDate not supplied

Overexpression of low density lipoprotein receptor on Chinese hamster ovary cells generates foam cells.

The atherosclerotic lesion is characterized by the presence of cholesterol-loaded foam cells. Chinese hamster ovary (CHO) cells do not normally store cholesteryl esters because low density lipoprotein (LDL) receptors are suppressed by exposure of these cells to LDL cholesterol. We transfected LDL receptor cDNA linked to the simian virus 40 early promoter into CHO cells (CHO 29) and found that LDL receptor binding in these cells was not suppressed by an excess amount of LDL cholesterol, indicating no regulation of the LDL receptor in CHO 29 cells. Furthermore, CHO 29 cells showed a high activity of LDL uptake and intracellular accumulation of cholesteryl esters. Light-microscopic examination demonstrated the resulting formation of foam cells in CHO 29 cells in the presence of 5 micrograms LDL/ml. These results demonstrated that foam cell changes in atherosclerotic lesions can be reproduced in CHO cells, whose LDL receptor activity is overexpressed, through the mechanism of LDL receptor-mediated endocytosis of native LDL.

Animals↗
PubMed1991

THP-1 cells form foam cells in response to coculture with lipoproteins but not platelets.

The human monocytic leukemia cell line, THP-1, shares many properties with human monocyte-derived macrophages and might be a useful model for studying foam cell formation in vitro. Therefore, we examined the ability of THP-1 cells to accumulate cholesteryl esters, the hallmark feature of foam cells, in response to culture with native low density lipoprotein (LDL), modified LDL, and platelets. THP-1 cells stored more cholesteryl esters than macrophages in response to 200 micrograms/ml of LDL. Down-regulation of LDL receptors occurred in macrophages at lower LDL concentrations than in THP-1 cells. Phorbol ester-treated THP-1 cells stored more cholesteryl esters than human macrophages in response to 25-200 micrograms/ml of acetylated LDL. Because we have previously demonstrated that activated platelets enhanced macrophage cholesteryl ester storage, we examined the ability of THP-1 cells to store cholesteryl esters in response to coculture with platelets. Compared with macrophages, dividing THP-1 cells and phorbol ester-treated THP-1 cells accumulated only 50% and 33% as much cholesteryl esters, respectively. Furthermore, although platelets induced a 90% reduction in cholesterol synthesis in macrophages by day 5, cholesterol synthesis in THP-1 cells and phorbol ester-treated THP-1 cells was inhibited less than 50% by platelets. Nevertheless, both THP-1 cells and macrophages responded to platelets by increasing their secretion of apolipoprotein E. Therefore, we conclude that dividing THP-1 cells and phorbol ester-treated THP-1 cells are capable of forming foam cells in response to physiologic doses of both LDL and acetylated LDL, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins E↗
PubMed1984

In situ characterization of the foam cells in early human atherosclerotic lesions.

Erythrocytes (E) sensitized with IgG antibodies bound to the fatty streaks in cryostat sections of early human atherosclerotic lesions. E sensitized with IgA or IgM antibodies of F(ab') 2 fragments of IgG did not bind. The binding was inhibited by intact IgG and by Fc fragments but not by F (ab')2 fragments or by albumin, indicating the presence of receptors for the Fc part of IgG (FcR). E sensitized with IgM antibodies and human complement did not bind. The FcR were also studied using soluble immune complexes of horseradish peroxidase (HRP) and rabbit IgG antibodies to HRP. The peroxidase activity was detected histochemically. The bound complexes were localized to most of the lipid cells (foam cells) in the lesions. The cytoplasm of the FcR positive foam cells stained diffusely for acid alpha- naphthyl acetate esterase. Most of the foam cells were stained with monoclonal antibodies against HLA-DR antigens. The data indicate that most foam cells in early atherosclerotic lesions are derived from monocytes.

Adult↗
PubMed1990

High-density-lipoprotein-induced cholesterol efflux from arterial smooth muscle cell derived foam cells: functional relationship of the cholesteryl ester cycle and eicosanoid biosynthesis.

Eicosanoids have been implicated in the regulation of arterial smooth muscle cell (SMC) cholesteryl ester (CE) metabolism. These eicosanoids, which include prostacyclin (PGI2), stimulate CE hydrolytic activities. High-density lipoproteins (HDL), which promote cholesterol efflux, also stimulate PGI2 production, suggesting that HDL-induced cholesterol efflux is modulated by eicosanoid biosynthesis. To ascertain the role of endogenously synthesized eicosanoids produced by arterial smooth muscle cells in the regulation of CE metabolism, we examined the effects of cyclooxygenase inhibition on CE hydrolytic enzyme activities, cholesterol efflux, and cholesterol content in normal SMC and SMC-derived foam cells following exposure to HDL and another cholesterol acceptor protein, serum albumin. Alterations of these activities were correlated with cholesterol efflux in response to HDL or bovine serum albumin (BSA) in the presence or absence of aspirin. HDL stimulated PGI2 synthesis and CE hydrolases in a dose-dependent manner. Eicosanoid dependency was established by demonstrating that HDL-induced acid cholesteryl ester hydrolase (ACEH) activity was blocked by aspirin. CE enrichment essentially abrogated HDL-induced PGI2 production in cells which also exhibited decreased lysosomal and cytoplasmic CE hydrolase activities. In CE-enriched cells whose cytoplasmic CE pool was metabolically labeled with [3H]oleate or cLDL containing [3H]cholesteryl linoleate, aspirin did not alter HDL- or BSA-induced net CE hydrolysis or efflux, respectively. Finally, aspirin treatment did not alter the mass of either free or esterified cholesterol content of untreated or CE-enriched SMC following exposure to acceptor proteins. These data demonstrated that CE enrichment significantly reduced HDL-induced activation of CE hydrolytic activity via inhibition of endogenous PGI2 production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The relationship between pre-existing subendothelial smooth muscle cell accumulations and foam cell lesions in cholesterol-fed rabbits.

We investigated whether pre-existing subendothelial smooth muscle cell (SMC) accumulations in cholesterol-fed rabbits are transformed into foam cell plaques. Twenty-four rabbits received a standard diet supplemented with 2% cholesterol for 4 or 8 weeks. Six rabbits received a supplement of 0.3% cholesterol for 35 weeks. The aorta and other systemic and pulmonary vessels were studied by immunohistochemistry for smooth muscle cells SMC (alpha-SMC actin), macrophages (RAM11), cell replication (proliferating cell nuclear antigen) and endothelial cells (von Willebrand factor; vWF). Initially the foam cell plaques were composed exclusively of foam cells of macrophage origin (MFC). In more advanced lesions SMC and collagen fibres were also present, leading to a fibrous transformation of the plaque. Cell replication was mainly located in the MFC. The endothelial cells covering the plaques showed an increased immunoreactivity for vWF which was also deposited in the interstitium between the FC. Pre-existing subendothelial SMC did not transform into FC. The newly formed FC plaques remained clearly separated from the pre-existing subendothelial SMC. The development of the plaques can be attributed not only to monocyte recruitment but also to macrophage multiplication.

Animals↗
PubMed1996

[Clinicopathological study of interstitial foam cells in idiopathic membranous nephropathy. Consideration of the appearance of interstitial foam cells in renal tissue].

We conducted an immunohistological investigation on the pathogenesis of interstitial foam cell formation in patients with idiopathic membranous nephropathy (MN). The patients were divided into two groups: Group I consisted of 23 MN patients with interstitial foam cells; Group II consisted of the other 159 patients without foam cells. Age at renal biopsy, duration of proteinuria, blood pressure and other clinical parameters were not significantly different between the two groups. The proportion of nephrotic patients in Group I was 52.2% (12/23), and was not significantly different from that in Group II (48.4%, 77/159). Renal biopsy specimens were examined by immunoperoxidase studies using monoclonal antibodies. The interstitial foam cells were positive for EBM11 (CD68) and 25F9, which are markers of macrophage (M phi) and mature M phi, respectively, but did not express markers of T cells. In interstitial infiltrating cells, both M phi and T cells were observed, but mature M phi were seldom seen. Furthermore, LFA-1 and ICAM-1, but not ICAM-3 (the third ligand for LFA-1) were observed in the interstitial foam cells. LFA-1 and ICAM-3 were observed mainly in interstitial infiltrating cells, but ICAM-1 was observed to a much lesser extent in these cells. These results suggest that interstitial foam cells in MN may be independent of severe hyperlipidemia and proteinuria, and that there may be different mechanisms underlying the accumulation of interstitial foam cells and infiltrating m phi s. Further investigations are required to clarify the pathogenesis of interstitial foam cells in renal tissue.

Female↗
PubMed1993

LDL inhibits the mediation of cholesterol efflux from macrophage foam cells by apoA-I-containing lipoproteins. A putative mechanism for foam cell formation.

Although the accumulation of cholesterol in macrophages appears to be an initial step in atherogenesis, low-density lipoprotein (LDL), a major risk factor for atherosclerosis, does not promote cholesterol accumulation in macrophages in its native form. On the other hand, apolipoprotein (apo) A-I-containing lipoprotein removes cholesterol from cholesterol-loaded macrophages (foam cells) and prevents cholesterol from accumulating in the cells. We examined the effect of LDL on cholesterol removal by two species of apoA-I-containing lipoproteins, one containing only apoA-I (LpA-I) and the other containing apoA-I and apoA-II (LpA-I/A-II). When foam cells were incubated with LpA-I or LpA-I/A-II, cellular cholesterol mass was reduced. In contrast, when LDL was added, the cholesterol-reducing capacities of these lipoproteins were dose-dependently inhibited by LDL. In the presence of LDL, LpA-I and LpA-I/A-II removed free cholesterol preferentially from LDL rather than from the plasma membrane of foam cells. In addition, a fair amount of cellular cholesterol was directly moved to LDL rather than to LpA-I or LpA-I/A-II. The cellular cholesterol that moved to LDL was completely compensated for by the cholesterol influx from LDL to foam cells. Thus, net cholesterol efflux (a combination of influx and efflux) from foam cells was inhibited by LDL. These results, taken together, indicate that LDL may accelerate foam cell formation by inhibiting cholesterol removal from the cells and that elevated levels of plasma LDL may become a risk factor for atherosclerosis by inhibiting the function of LpA-I and LpA-I/A-II at the cellular level.

Animals↗
PubMed1998

Human peritoneal monocytic cells: lipoprotein uptake and foam cell formation.

Human peritoneal cells isolated from dialysis effluent have in vivo maturated human macrophages that could serve as a model for studying lipoprotein metabolism and foam cell formation. We previously characterized the low density lipoprotein (LDL) and acetylated LDL (acetyl-LDL) receptor activities of human total peritoneal cells. Now, we provide evidence that both LDL and acetyl-LDL stimulate acylCoA cholesterol:acyl transferase (ACAT) activity of peritoneal cells. Prolonged incubation of cells with LDL results in suppression of ACAT activity, while incubation with acetyl-LDL results in elevated and sustained enzyme activity. When human peritoneal cells were analyzed using flow cytometry, the cell population showed reactivity for CD2, CD4, CD8, CD20, CD14 and HLA-DR antigens. Purified human peritoneal mononuclear cells degraded LDL. Human peritoneal macrophages formed foam cells when exposed to LDL or acetyl-LDL in culture, and lipid deposition increased with incubation time. Macrophages incubated in the presence of butylated hydroxy toluene and LDL did not form foam cells.

Foam Cells↗
PubMed1975

Drug-induced foam cell reactions in rats, II. Chemical analysis of lipids stored in lungs and foam cells after treatment with chlorphentermine, 5-[p-(fluoren-9-ylidenemethyl)phenyl]-2-piperidineethanol (RMI 10.393) and 1-chloramitriptyline.

Lipidosis and foam cell reaction was induced in rat lungs by repeated administration of chlorphentermine, RMI 10.393 (=5-[p-(fluoren-9-ylidenemethyl)phenyl]-2-piperidineethanol), and 1-chloramitriptyline. Foam cell and lung lipids were extracted and separated in classes by thin-layer chromatography. Phospholipids were determined by phosphorus analysis, while neutral lipids were measured densitometrically. In lungs of drug-treated rats lecithin, phosphatidyl glycerol, phosphatidic acid, phosphatidyl inositol and free fatty acids accumulated in varying amounts. All other lipids were present in normal or reduced concentrations. Foam cells of chlorphentermine- and RMI 10.393-treated rats contained mainly phospholipids, i.e. lecithin and only small amounts of neutral lipids, i.e. cholesterol. Foam cells induced by 1-chloramitriptyline contained besides phospholipids also large amounts of neutral lipids, i.e. cholesterol, free fatty acids and cholesterol esters. This study and recent reports of others show that certain drugs produce a generalized metabolic disturbance characterized by accumulation of various lipids in several tissues. The distribution patterns of lipids induced by various drugs may differ considerably. This indicates that several biochemical mechanisms may be involved in the pathogenesis of drug-induced lipidosis.

Amitriptyline↗
PubMed1995

T helper cell infiltration and foam cell proliferation are early events in the development of atherosclerosis in cholesterol-fed rabbits.

The involvement of T cells in the early cellular events in atherosclerosis was studied in rabbits fed a 1% cholesterol diet by use of specific monoclonal anti-rabbit CD5 and CD4 antibodies. T cells were not seen in the aortic intimas of rabbits not fed cholesterol but were seen in intimal lesions in cholesterol-fed rabbits. Accumulation of T cells in plaques occurred between 2 and 4 weeks after commencement of cholesterol feeding, and the greatest density of CD5-positive T cells were observed after 4 weeks (11.2 +/- 6.0 cells/mm2 [mean +/- SEM]; P < .02 compared with normal control rabbits, P < .03 compared with 2-week plaques). Staining for CD4 indicated that the majority of these T cells were T helper cells (9.9 +/- 4.9 cells/mm2). At this time, plaques showed a dense cellular infiltrate of macrophages (3623 +/- 467 cells/mm2) and macrophage proliferation was evident (2.1 +/- 1.1% of total plaque cells). As the cross-sectional area of intimal lesions increased progressively in subsequent weeks, their cellularity declined (8 weeks, 2239 +/- 271 cells/mm2; 12 weeks, 1535 +/- 55 cells/mm2; 16 weeks, 1747 +/- 242 cells/mm2, P < .05 for all groups compared with the 4-week group). The density of the T cell infiltrate (8 weeks, 6.7 +/- 3.0 cells/mm2; 12 weeks, 0.6 +/- 0.2 cells/mm2; 16 weeks, 1.0 +/- 0.4 cells/mm2) and the proliferative index of cells within plaques (8 weeks, 0.6 +/- 0.2%; 12 weeks, 0.8 +/- 0.3%; 16 weeks, 0.2 +/- 0.2%) also declined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

The importance of smooth muscle cells in the development of foam cells in the gastric mucosa. An electron microscopic study.

Foam cells in lipid islands of the stomach can develop from both histiocytes and smooth muscle cells. With increasing storage of lipid vacuoles in smooth muscle cells, loosening of the myofilament arrangement and decrease of the dense areas subjacent to the plasma membrane occurs. Endoplasmic reticulum and the cisternae of the Golgi-apparatus dilate, the cell organelles increase initially and the basement membrane of the smooth muscle cells is fragmentarily formed. Only in incompletely formed foam cells can the origin from smooth muscle cells be recognised, in their final state their histiogenesis is seldom apparent.

Aged↗
PubMed1987

Agglomeration to nodules modulates human arterial smooth muscle cells to distinct postinjury phenotype via foam cell transition.

Cultures of arterial smooth muscle cells (SMCs) tend to form loci with multilayered growth as "hills" or "nodules," which is unusual for normal but common for transformed cells. Earlier it was shown that such nodules were composed of SMCs with the distinctive properties of small cell size, low adhesivity, and scarce or no fibronectin and filamentous actin, features which may also characterize tumor cells. Similar properties could be induced by cultivation of SMCs in aggregates, indicating modulation of SMCs to a distinct "multilayered" phenotype, rather than selection of variant SMCs with preference for multilayered growth. Transfer of SMCs to a three-dimensional arrangement by agglomeration to nodules, "spheroids," by seeding of SMCs on low-adhesive substratum, like agarose, was followed by signs of SMC injury with focal autodigestion and with loss of material from the cells, which to some extent was deposited extracellularly, transition to foam cells with cholesterol accumulation mainly as cholesteryl esters, and eventually decrease in cell size. Identically treated fibroblasts showed similar, but much less pronounced, changes and were largely protected by whole blood serum, in contrast to SMCs. The results indicate that the "multilayered" SMC type can be conceived of as a postinjury phenotypic state which is preceded by overt cellular injury and transition to foam cells in conjunction with sudden transfer to three-dimensional arrangement in spheroids. It is suggested that similar modulation may be important in atherosclerosis, in which foam cell transition and deposition of debris are prominent changes.

Cell Adhesion↗
PubMed1997

Regulation, location and activity of plasminogen activator inhibitor 2 (PAI-2) in peripheral blood monocytes, macrophages and foam cells.

Monocytes, macrophages and foam cells are central to atherogenesis. We have examined the potential ability of monocytes, macrophages and foam cells to affect the stability of deposited fibrin, characteristic of the atherosclerotic plaque, by their production of plasminogen activators and their inhibitors. Monocytes respond to thrombin and LPS by up-regulation of PAI-2 synthesis, and PAI-2 is their major product among the plasminogen activators/inhibitors. In contrast, macrophages and foam cells, while they did produce PAI-2, did not respond to thrombin and LPS by an increase in its synthesis. All PAI-2 produced by macrophages and foam cells was accumulated intracellularly, whereas monocytes also secreted PAI-2. Secreted PAI-2 was active as an inhibitor of u-PA, whereas intracellular PAI-2 required detergent treatment to generate activity. Thus monocytes, but not macrophages or foam cells, produce and secrete active PAI-2, thus potentially affecting fibrin stability in the local environment.

Cells, Cultured↗
PubMed1993

Lipoprotein-proteoglycan complexes induce continued cholesteryl ester accumulation in foam cells from rabbit atherosclerotic lesions.

We studied the metabolism of lipoprotein-proteoglycan complexes by macrophage-derived foam cells. Foam cells were isolated from atherosclerotic rabbit aortas. ApoB-lipoprotein-proteoglycan complex was isolated from human aorta fibrous plaque lesions and LDL-proteoglycan complex was formed in vitro. Both in vitro and in vivo complexes stimulated cholesteryl ester synthesis in foam cells by a dose-dependent, saturable process that resulted in the intracellular accumulation of cholesteryl ester. Stimulation of cholesteryl ester synthesis was linear with time over a 32-h period. Polyinosinic acid inhibited the stimulation of cholesteryl ester synthesis by the complexes by 32-37%, whereas cytochalasin D only produced a 6-16% inhibition. Foam cells degraded 125I-LDL-proteoglycan complex and 125I-acetyl LDL in a saturable, dose-dependent manner. Excess unlabeled acetyl-LDL inhibited the degradation of 125I-LDL-proteoglycan complex by 52%, while LDL had no effect. Similarly, excess unlabeled complex suppressed the degradation of 125I-acetyl-LDL by 48%. Foam cells degraded 125I-methyl-LDL-proteoglycan complex to the same extent as 125I-LDL-proteoglycan complex. These results show that foam cells from atherosclerotic lesions metabolize lipoprotein-proteoglycan complexes predominantly via receptor-mediated endocytosis and consequently continue to accumulate intracellular cholesteryl ester.

Animals↗
PubMed1998

Induction of macrophage foam cell formation by Chlamydia pneumoniae.

Foam cell formation is the hallmark of early atherosclerosis. It was found that the intracellular bacterium Chlamydia pneumoniae induces foam cell formation by human monocyte-derived macrophages. Exposure of macrophages to C. pneumoniae followed by low-density lipoprotein (LDL) caused a marked increase in the number of foam cells and accumulation of cholesteryl esters. Foam cell formation was not inhibited by the antioxidant butylated hydroxytoluene nor fucoidan, suggesting that lipid accumulation did not involve scavenger receptors. In contrast, addition of heparin, which blocks binding of LDL to the LDL receptor, inhibited C. pneumoniae-induced foam cell formation, suggesting that the pathogen induced lipid accumulation by dysregulating native LDL uptake or metabolism (or both). These data demonstrate that an infectious agent can induce macrophage foam cell formation and implicate C. pneumoniae as a causative factor in atherosclerosis.

Arteriosclerosis↗
PubMed1993

Mammary ductal foam cells: macrophage immunophenotype.

Mammary ductal foam cells are present in normal breast tissue as well as in a number of breast diseases. Such foam cells tend to be in particular abundance with fibrocystic changes of the breast. Foam cells may appear within duct lumens or plastered in cohesive masses along duct walls, simulating an epithelial structure. The nature and origin of these innocuous-appearing cells, based on morphologic studies, remain a controversy, for they appear to be of epithelial derivation. This study was undertaken to determine the nature of intraductal "foam" cells and their origin in the breast. Nine cases of adult fibrocystic disease were examined immunohistochemically with antibodies to cytokeratins (Mak-6, Cam 5.2), leukocyte common antigen, and the following macrophage antibodies: KP-1 (CD68), HAM 56, and MAC 387. The lysozyme and alpha-1-antitrypsin content of foam cells also was studied. The immunohistochemical data in this study confirm the macrophage character of these foam cells, which are positive for CD68, HAM 56, and MAC 387, lysozyme, and alpha-1-antitrypsin and negative for leukocyte-common antigen and cytokeratins.

Antibodies↗