Induction of interleukin‐1 receptors on chondrocytes by fibroblast growth factor: A possible mechanism for modulation of interleukin‐1 activity
Identifieur interne : 003168 ( Main/Exploration ); précédent : 003167; suivant : 003169Induction of interleukin‐1 receptors on chondrocytes by fibroblast growth factor: A possible mechanism for modulation of interleukin‐1 activity
Auteurs : Srinivasan Chandrasekhar [États-Unis] ; Anita K. Harvey [États-Unis]Source :
- Journal of Cellular Physiology [ 0021-9541 ] ; 1989-02.
English descriptors
- Teeft :
- Acad, Acidic, Additional receptors, Afgf, Arthritis rheum, Articular, Articular cartilage, Basic fibroblast growth factor, Bfgf, Binding buffer, Biochem, Biol, Biological activity, Bovine, Bovine serum albumin, Cartilage, Cell biol, Chandrasekhar, Chloroquine, Chondrocytes, Cluster plates, Collagenase, Confluency, Dmem, Fgfs, Fibroblast, Fibroblast growth factor, Growth factor, Growth factors, Heparin, Interleukin, Intracellular processing, Link protein, Macrophage, Natl, Neutral protease, Neutral protease activity, Ngiml, Nucleotide sequence, Phadke, Potentiate, Potentiation, Previous studies, Proc, Protease, Protease activity, Protease production, Protease secretion, Proteoglycan, Rabbit articular chondrocytes, Radiolabeled, Receptor, Receptor number, Recombinant, Results show, Saklatvala, Single class, Specific activity, Specific binding, Synovial, Treatment time, Various concentrations, Wound repair.
Abstract
Interleukin‐1 is a polypeptide factor with profound effects on several cell types, such as chondrocytes, fibroblasts, and T‐cells. The ability of interleukin‐1 to induce the synthesis of matrix‐degradative enzymes, as well as prostangladin E2, suggests a pivotal role for this mediator in chronic inflammation. Previous studies have shown that the effect of human monocyte interleukin‐1 on the synthesis of collagenase and neutral proteases by chondrocytes was enhanced by basic fibroblast growth factor. Using recombinant human interleukin‐1 B, we have examined whether the potentiation of interleukin‐1 effects by fibroblast growth factor is related to changes in the number or affinity of interleukin‐1 receptors. Our studies confirm that rabbit articular chondrocytes in culture contain a single class of high‐affinity receptors for interleukin‐1 with a Ka of 0.9–1.1 × 10– 13M–1While the untreated chondrocytes contain approximately 1,620 receptors per cell, fibroblast growth factor‐treated cells exhibit a higher number of receptors (approximately 2,960 per cell) with no apparent change in the affinity. The increase in receptor number can be abolished by inhibitors of lysosomal function, indicating a requirement for intracellular processing of the fibroblast growth factor. Our results suggest that the potentiation of interleukin‐1 catabolic effects by fibroblast growth factor may be related to its ability to induce additional interleukin‐1 receptors on the chondrocyte cell surface.
Url:
DOI: 10.1002/jcp.1041380204
Affiliations:
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Induction of interleukin‐1 receptors on chondrocytes by fibroblast growth factor: A possible mechanism for modulation of interleukin‐1 activity</title><author><name sortKey="Chandrasekhar, Srinivasan" sort="Chandrasekhar, Srinivasan" uniqKey="Chandrasekhar S" first="Srinivasan" last="Chandrasekhar">Srinivasan Chandrasekhar</name></author><author><name sortKey="Harvey, Anita K" sort="Harvey, Anita K" uniqKey="Harvey A" first="Anita K." last="Harvey">Anita K. 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Harvey</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Indiana</region></placeName><wicri:cityArea>Department of Connective Tissue and Monoclonal Antibody Research, Lilly Research Laboratories, Building 98C/4, Lilly Corporate Center, Indianapolis</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Cellular Physiology</title><title level="j" type="alt">JOURNAL OF CELLULAR PHYSIOLOGY</title><idno type="ISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><imprint><biblScope unit="vol">138</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="236">236</biblScope><biblScope unit="page" to="246">246</biblScope><biblScope unit="page-count">11</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1989-02">1989-02</date></imprint><idno type="ISSN">0021-9541</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acad</term><term>Acidic</term><term>Additional receptors</term><term>Afgf</term><term>Arthritis rheum</term><term>Articular</term><term>Articular cartilage</term><term>Basic fibroblast growth factor</term><term>Bfgf</term><term>Binding buffer</term><term>Biochem</term><term>Biol</term><term>Biological activity</term><term>Bovine</term><term>Bovine serum albumin</term><term>Cartilage</term><term>Cell biol</term><term>Chandrasekhar</term><term>Chloroquine</term><term>Chondrocytes</term><term>Cluster plates</term><term>Collagenase</term><term>Confluency</term><term>Dmem</term><term>Fgfs</term><term>Fibroblast</term><term>Fibroblast growth factor</term><term>Growth factor</term><term>Growth factors</term><term>Heparin</term><term>Interleukin</term><term>Intracellular processing</term><term>Link protein</term><term>Macrophage</term><term>Natl</term><term>Neutral protease</term><term>Neutral protease activity</term><term>Ngiml</term><term>Nucleotide sequence</term><term>Phadke</term><term>Potentiate</term><term>Potentiation</term><term>Previous studies</term><term>Proc</term><term>Protease</term><term>Protease activity</term><term>Protease production</term><term>Protease secretion</term><term>Proteoglycan</term><term>Rabbit articular chondrocytes</term><term>Radiolabeled</term><term>Receptor</term><term>Receptor number</term><term>Recombinant</term><term>Results show</term><term>Saklatvala</term><term>Single class</term><term>Specific activity</term><term>Specific binding</term><term>Synovial</term><term>Treatment time</term><term>Various concentrations</term><term>Wound repair</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Interleukin‐1 is a polypeptide factor with profound effects on several cell types, such as chondrocytes, fibroblasts, and T‐cells. The ability of interleukin‐1 to induce the synthesis of matrix‐degradative enzymes, as well as prostangladin E2, suggests a pivotal role for this mediator in chronic inflammation. Previous studies have shown that the effect of human monocyte interleukin‐1 on the synthesis of collagenase and neutral proteases by chondrocytes was enhanced by basic fibroblast growth factor. Using recombinant human interleukin‐1 B, we have examined whether the potentiation of interleukin‐1 effects by fibroblast growth factor is related to changes in the number or affinity of interleukin‐1 receptors. Our studies confirm that rabbit articular chondrocytes in culture contain a single class of high‐affinity receptors for interleukin‐1 with a Ka of 0.9–1.1 × 10– 13M–1While the untreated chondrocytes contain approximately 1,620 receptors per cell, fibroblast growth factor‐treated cells exhibit a higher number of receptors (approximately 2,960 per cell) with no apparent change in the affinity. The increase in receptor number can be abolished by inhibitors of lysosomal function, indicating a requirement for intracellular processing of the fibroblast growth factor. Our results suggest that the potentiation of interleukin‐1 catabolic effects by fibroblast growth factor may be related to its ability to induce additional interleukin‐1 receptors on the chondrocyte cell surface.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Indiana</li></region></list><tree><country name="États-Unis"><region name="Indiana"><name sortKey="Chandrasekhar, Srinivasan" sort="Chandrasekhar, Srinivasan" uniqKey="Chandrasekhar S" first="Srinivasan" last="Chandrasekhar">Srinivasan Chandrasekhar</name></region><name sortKey="Chandrasekhar, Srinivasan" sort="Chandrasekhar, Srinivasan" uniqKey="Chandrasekhar S" first="Srinivasan" last="Chandrasekhar">Srinivasan Chandrasekhar</name><name sortKey="Harvey, Anita K" sort="Harvey, Anita K" uniqKey="Harvey A" first="Anita K." last="Harvey">Anita K. Harvey</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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