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Biomedical subjects

R Y Ball

Publications and source records attributed to R Y Ball.

At least 55 records · Page 3Linked to original sources
PubMed1990

Macrophages and ceroid in human atherosclerosis.

It is proposed that atherosclerosis is a chronic inflammatory disease in which monocyte-derived macrophages are doing harm and smooth muscle cells are essentially reparative. Activities of macrophages that might be contributory to the development of atherosclerosis are tabulated. Observations and experiments are described that suggest macrophages may be contributing to lipoprotein oxidation within the plaque and that individual humans vary in their macrophage oxidative capacity. The possibility of intervention with antioxidants is discussed.

Animals↗
PubMed1990

Ceroid accumulation by murine peritoneal macrophages exposed to artificial lipid-containing particles: the role of the hydrophilic component.

Murine resident peritoneal macrophages were maintained in cell culture in a medium containing 10% lipoprotein-deficient foetal calf serum to which various artificial lipid-containing particles were added. These had a core of oxidizable lipid, generally cholesteryl linoleate, and were stabilized in aqueous suspension by one of a variety of poly-L-amino acids, proteins or polysaccharides. Most particles, except those containing poly-L-lysine or poly-L-arginine (both strongly basic), were readily taken up by the macrophages to form typical ceroid inclusions, the morphological form of which was determined by the nature of the core lipid. The hydrophilic stabilizing component seemed largely irrelevant in this respect. The role of the latter appears largely to be to allow the cellular uptake of lipid, although it may also participate in ceroid formation.

Animals↗
PubMed1989

Modulation of ceroid accumulation in macrophages in vitro.

Mouse resident peritoneal macrophages (MPM) cultured with artificial lipoprotein consisting of cholesteryl linoleate complexed with bovine serum albumin (CL/BSA) rapidly accumulate ceroid in the form of rings. Experiments with various phenolic radical scavenger antioxidants and derivatives showed that the radical scavengers which are strongly lipophilic, and possess a free (i.e. non-esterified) phenolic hydroxyl group are inhibitors of ceroid ring formation. Time-course experiments with MPM and CL/BSA in which either or both of the components of the artificial lipoprotein have been oxidised before feeding showed that such oxidation accelerated ceroid accumulation, and suggested that oxidation of the lipoprotein is rate-determining in ceroid accumulation. Copper appeared to be a good catalyst for this. Agents able to activate the respiratory burst production of reactive oxygen species appeared to have no accelerating effect on ceroid accumulation from CL/BSA by MPM in a time-course. A novel method has been attempted for quantitating ceroid in MPM by means of its autofluorescence, using a Fluorescence-activated Cell Sorter (FACS). The results from FACS agree qualitatively with those from alcohol-xylene treatment followed by oil-red-o staining (AX/ORO). MPM cultured with CL/BSA for up to 4 days showed a 2.7-4.6-fold increase in mean fluorescence (at wavelengths greater than 490 nm) over MPM cultured with cholesteryl oleate/BSA (CO/BSA), with CL/BSA/butylated hydroxytoluene (CL/BSA/BHT), with CL/BSA/probucol, and with no artificial lipoprotein. The implications of the findings with respect to human atherosclerosis are discussed.

Animals↗
PubMed1989

Saccharide expression on wounded endothelial cell monolayers in vitro.

Monolayer cultures of porcine aortic endothelial cells were used as a model of the endothelium of large arteries. Linear wounds were produced in such cultures by scraping and the subsequent sequence of events in nearby cells was analysed. The earliest detectable event was cellular spreading at the margins of the wounds (2 h) followed by cell migration (starting at 6-8 h) and cell proliferation in regions adjacent to the wound (16 h and later). Cell spreading was associated with the appearance of saccharides selectively at the spreading margins of the cells, which bound the lectins, ConA, LCA and PSA, and were sensitive to alpha-mannosidase. Terminal alpha-mannosyl residues were therefore present. The appearance of these saccharides suggests a mechanism by which monocytes might adhere to and/or migrate through the endothelium of vessels at sites of cellular response to injury.

Animals↗
PubMed1988

Ceroid accumulation by murine peritoneal macrophages exposed to artificial lipoproteins: ultrastructural observations.

Murine resident peritoneal macrophages were maintained in cell culture in a medium containing 10% lipoprotein-deficient fetal calf serum to which various artificial lipoprotein particles (coacervates of lipid and bovine serum albumin) had been added. The uptake and intracellular fate of these particles was studied by electron microscopy. The appearance of material accumulating within the cells varied according to the nature of the lipid component of the ingested particles. Lipids which are readily oxidised (cholesteryl linoleate, cholesteryl arachidonate, trilinolein) were associated with the formation of ceroid within membrane-bound structures. Less readily oxidized lipids (cholesteryl oleate, triolein) were not associated with ceroid accumulation but instead the cells contained numerous nonmembrane-bound lipid inclusions. The appearances of the ceroid within the murine peritoneal macrophages are similar to those of ceroid in macrophages in human atherosclerotic lesions.

Animals↗
PubMed1987

What is the significance of ceroid in human atherosclerosis?

This review of the significance of ceroid within the atherosclerotic intima proposes that the macrophages have a central role to play in its production. Ceroid is more than merely an "age pigment." It marks the site of previous oxidative events, possibly including the release of biologically active or toxic, soluble oxidized molecules. This being so, this activity of macrophages may have a significant role in the progression of the lesions. The interactions of macrophages and oxidizable unsaturated lipids therefore merit further investigation.

Animals↗
PubMed1987

Ceroid accumulation by murine peritoneal macrophages exposed to artificial lipoproteins.

Murine resident peritoneal macrophages were maintained in cell culture in a medium containing 10% lipoprotein-deficient fetal calf serum to which various artificial lipoproteins (lipid-bovine serum albumin complexes) had been added. Ceroid accumulated in cells exposed to artificial lipoproteins containing cholesteryl esters or acylglycerols possessing polyunsaturated fatty acid residues, but not in cells exposed to lipoproteins containing less readily oxidized lipids. Oxidation of cholesteryl linoleate before its incorporation into artificial lipoprotein accelerated ceroid production. Incorporation of free radical scavengers into cholesteryl linoleate-containing artificial lipoproteins impaired ceroid formation. The results are discussed in terms of the mechanisms by which the ceroid might have been produced and its significance for human atherogenesis.

Animals↗
PubMed1986

Oxidized low density lipoprotein induces ceroid accumulation by murine peritoneal macrophages in vitro.

The presence of ceroid pigment inclusions within macrophage foam cells is a well-recognized phenomenon in human atherosclerosis but its significance is unclear. Murine peritoneal macrophages, maintained in a medium containing 10% lipoprotein-deficient fetal calf serum to which oxidized low density lipoprotein (LDL) has been added, rapidly accumulate similar ceroid inclusions. However, cells exposed to LDL, acetyl--LDL or dextran sulphate--LDL complexes fail to develop ceroid under the same culture conditions. Oxidation of LDL results in considerable physico-chemical changes to both protein and lipid moieties, and these may be important in the uptake of the particles by macrophages and, subsequently, the accumulation of intracellular ceroid.

Animals↗
PubMed1985

Identification of macrophages and smooth muscle cells in human atherosclerosis using monoclonal antibodies.

Sections of human atherosclerotic plaques were stained by the indirect immunoperoxidase technique using three rat anti-human monoclonal antibodies: YAML 501.4 (anti-'leukocyte-common' (T200) antigen; YTH 8.18 (antimacrophage cytoplasm); and YPC 1/3 . 12 (anti-smooth muscle cell). The cells of diffuse intimal thickening were almost all smooth muscle cells but there were rare subendothelial macrophages. Focal lesions, in contrast, contained numerous macrophages as well as smooth muscle cells. Macrophage 'foam cells' were particularly numerous in fatty streaks and in advanced fibro-fatty plaques, but were less conspicuous in focal fibro-elastic lesions. The results confirm that macrophages are an important component of atherosclerotic plaques and suggest that they may have a significant role in atherogenesis in man.

Adult↗
PubMed1984

Monocytic origin of foam cells in human atherosclerotic plaques.

Foam cells in 4 human atherosclerotic plaques reacted with 3 rat monoclonal antibodies directed against T.200 ('anti-leucocyte common' antibody), HLA-Class II molecules and macrophage cytoplasm, respectively. Smooth muscle cells did not react. The results support the view that foam cells are monocyte-derived macrophages.

Adult↗
PubMed1984

Obstructive lesions of the genital tract in men.

Obstructive lesions of the efferent and epididymal ducts in man were a common finding at necropsy. Although they demonstrated evidence of resorption of spermatozoa, they did not appear to be associated with the development of spermagglutinating antibodies in most cases. It is concluded that local spermiophagy within the genital tract in men is insufficient to lead to the development of antisperm autoallergy as detected by the tray agglutination test.

Adolescent↗
PubMed1984

Further observations on spermiophagy by murine peritoneal macrophages in vitro.

Resident mouse peritoneal macrophages when maintained in cell culture phagocytosed and degraded homologous epididymal spermatozoa. The acrosome and its associated antigens were readily degraded, showing degenerative changes within minutes of spermiophagy and being completely destroyed by 1 h. Other components of the spermatozoon were more resistant and fragments of nuclear material and tail axial filaments could still be recognized within some macrophages up to 7 days after phagocytosis. The findings may be relevant to the disposal of spermatozoa in the genital tract in vivo.

Animals↗
PubMed1984

The production of ceroid by mouse peritoneal macrophages in vitro.

Murine resident peritoneal macrophages accumulated lipid droplets and subsequently insoluble, ceroid-like material when cultured in vitro in a medium containing 33% fetal calf serum. At least some of this insoluble lipid was membrane-bound and by light microscopy it often appeared as 'rings' with a hollow centre. It is suggested that the production of ceroid may be the consequence of the uptake of lipids from the extracellular medium and the activity of the macrophage's membrane-bound oxidative microbicidal mechanisms. The results indicate that macrophages are capable of rendering lipids insoluble, supporting the suggestion that this might occur in the atherosclerotic plaque.

Animals↗