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  • 1
    Electronic Resource
    Electronic Resource
    Effects of interleukin-1 on fibroblast extracellular matrix, using a 3-dimensional culture system (1989)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 139 (1989), S. 501-508 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: This study describes the alterations induced by Interleukin-1α and -β (IL-1α and IL-1β) on fibroblast-synthesized extracellular matrix. Fibroblasts were grown between pieces of dentin or in collagen-coated Terasaki wells for 3 or 6-9 weeks to create 3-dimensional cell-containing matrices constituted primarily of proteoglycans and collagens, respectively. Following incubation with IL-1α or IL-1β (10-9 M) at 37°C for 24 or 72 hr, samples were prepared for light and electron microscopy. Both IL-1α and IL-1β induced collapse of the extracellular matrix by 72 hr, as manifested by a decrease of the cross-sectional area and an increased density of the matrices. Three-week matrices were reduced 26% and 45% by using IL-1α and IL-1β, respectively. Comparable values obtained by using 6-week matrices were 14% and 30%. Cells within the matrix, normally stellate in shape with numerous extended processes, attained a more rounded or spindle shape with few and reduced processes and showed apparent alterations at cell matrix attachment sites and rearrangement of the cytoskeleton. Elongated cells at the top of the matrix appeared more compressed. The alterations were more pronounced in cultures incubated with IL-β than with IL-1α. Immunocytochemistry of extracellular matrix components revealed a decrease in staining intensity of chondroitin and dermatan sulfate in the 3-week matrix following IL-1β incubation. There was also a decrease in collagen type I staining of 9-week matrices treated with IL-1α or IL-1β. These studies show that IL-1 has an effect on fibroblast-synthesized extracellular matrix and indicate that the effects of IL-1α and IL-1β may differ. The resulting collapse of the matrix appears at least in part to be due to changes in proteoglycans and collagens.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041390308
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  • 2
    Electronic Resource
    Electronic Resource
    Expression and function of gingival fibroblast C1q receptors are upregulated by interleukin-1β and transforming growth factor-β (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 155 (1993), S. 157-163 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In injury and inflammation, complement (C) component C1q, in addition to its central role in initiation of classical pathway of complement activation, modulates diverse cellular functions by binding to specific cell surface receptors. Interaction of substrate-bound C1q with receptors for the collagen-like domain of C1q (C1qRC) of human gingival fibroblasts (HGF) promotes cell attachment. We investigated modulation of the adhesive function and expression of C1qRC by interleukin-1β (IL-1β) and transforming growth factor-β (TGF-β). Confluent fibroblast monolayers were incubated under standard culture conditions with or without cytokines. C1qRC function was measured by attachment assays. IL-1β and TGF-β increased fibroblast adhesion to C1q to 146% and 131% of controls, respectively. Cytokine enhancement of HGF adhesion was concentration-dependent, saturable (20 ng/ml IL-1β; 1 ng/ml TGF-β) and time-dependent (IL-1β 12-hr peak; TGF-β 24-hr peak). Effect of IL-1β and TGF-β on C1qRC expression was assessed by flow cytometry measurements of fluorescence intensity of cells stained with C1q and FITC anti-C1q antibody, and by binding studies with 125l-C1q. Cells treated with cytokines displayed a two- to four-fold increased fluorescence of cell-bound C1q compared to controls. Binding studies indicated the increased fluorescence correlated with increase in number of C1qRC in both IL-1β (4.7 × 106/cell) and TGF-β (3.9 × 106/cell)-treated cells, compared to control (3.0 × 106/cell), but had no effect on binding affinity. Rates of internalization of receptor-bound C1q were similar in cytokine-treated cells and controls. We propose from these data that IL-1β and TGF-β have the ability to upregulate C1qRC expression, and this effect contributes to increased adhesion of HGF to substrate-bound C1q. © 1993 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041550120
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  • 3
    Electronic Resource
    Electronic Resource
    Lipid peroxidation in purified plasma membrane fractions of rat liver in relation to the hepatoxicity of carbon tetrachloride (1988)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 6 (1988), S. 87-99 
    Details
    ISSN: 0263-6484
    Keywords: Carbon tetrachloride ; lipid peroxidation: plasma membrane ; liver injury ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Preparations of rat liver sinusoidal plasma membrane have been tested for their ability to metabolize the hepatotoxin carbon tetrachloride (CCl4) to reactive free radicals in vitro and compared in this respect with standard preparations of rat liver microsomes. The sinusoidal plasma membranes were relatively free of endoplasmic reticulum-associated activities such as the enzymes of the cytochrome P450 system and glucose-6-phosphatase. CCl4 metabolism was measured as (i) covalent binding of [14C]-CCl4 to membrane protein, (ii) electron spin resonance spin-trapping of CCl3· radicals and (iii) CCl4-induced lipid peroxidation. By all of these tests, purified sinusoidal plasma membranes were found unable to metabolize CCl4.The fatty acid composition of the plasma membranes was almost identical to that of the microsomal preparation and both membrane fractions exhibited similar rates of the lipid peroxidation that was stimulated non-enzymically by γ-radiation or incubation with ascorbate and iron. The absence of CCl4-induced lipid peroxidation in the plasma membranes seems to be due, therefore, to an absence of CCl4 activation rather than an inherent resistance to lipid peroxidation.We conclude that damage to the hepatocyte plasma membrane during CCl4 intoxication is not due to a significant local activation of CCl4 to CCl3· within that membrane.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290060203
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  • 4
    Electronic Resource
    Electronic Resource
    Carcinogenicity of CoCrMo (F-75) implants in the rat (1996)
    Hoboken, NJ : Wiley-Blackwell
    Journal of Biomedical Materials Research 32 (1996), S. 37-44 
    Details
    ISSN: 0021-9304
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine , Technology
    Notes: A long-term study was conducted in rats to assess the contribution of the surface area of CoCrMo devices to carcinogenesis. Groups consisting of 104 rats each (52 male, 52 female) were either implanted with metal cylinders fixed on the left, lateral femur (groups 1-3) or injected with a suspension of metal microspheres in the dorsal subcutis (group 4). Group 1 (control) received solid Ti6Al4V cylinders [surface area to body weight (SA/BW) ratio measuring 1.35 times that of human total hip prosthesis (HTHP)]. Group 2 was implanted with solid CoCrMo (SA/BW ratio: identical to implants of group 1). Group 3 received sintered-porous CoCrMo devices (SA/BW ratio: 30 × HTHP). Group 4 was injected with a suspension of CoCrMO microspheres (SA/BW ratio: 135 × HTHP). Implant-associated tumors (IATs) were observed in 23, 14, 3, and 15 rats of groups 1, 2, 3, and 4, respectively. Within groups 1 and 2, 34 IATs were associated with loose implants, three with undetermined implant fixation status, and none with fixed implants. A significantly increased accumulation of chronic inflammatory tissues around loose rather than fixed implants suggested a foreign-body reaction as the primary mechanism of carcinogenesis. A secondary role in carcinogenesis was ascribed to the increased CoCrMo implant SA/BW ratios as indicated by a 14.6% IAT incidence in group 4 versus 3% in group 3. These results support the notion that early intervention in the removal of loose metal devices is warranted to mitigate against foreign body-induced carcinogenesis, at least in this animal model. © 1996 John Wiley & Sons, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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