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   <subfield code="a">10.1007/s00011-011-0365-y</subfield>
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   <subfield code="a">Inflammatory effect of advanced glycation end products on human meniscal cells from osteoarthritic knees</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Hideki Hiraiwa, Tadahiro Sakai, Hirohito Mitsuyama, Takashi Hamada, Ryuichiro Yamamoto, Takaaki Omachi, Yohei Ohno, Motoshige Nakashima, Naoki Ishiguro]</subfield>
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   <subfield code="a">Objective: To investigate the inflammatory effects of advanced glycation end-products (AGEs) through the receptor for AGE in meniscal cells from osteoarthritic knees, and examine effects of hyaluronan (HA) on AGE-induced inflammation. Methods: Meniscal cells from human osteoarthritic knees were cultured with or without glycolaldehyde-AGE-bovine serum albumin and 800kDa HA. The amount of prostaglandin E2 (PGE2) protein was determined using an enzyme immunoassay system. Expression of cyclooxygenase (COX)-1, COX-2, membrane associated prostaglandin E synthase (mPGES)-1 and cytosolic PGES (cPGES) was analyzed by real-time reverse transcription polymerase chain reaction and western blotting. Results: PGE2 synthesis was significantly increased by AGEs, and AGE-induced PGE2 production was attenuated by addition of HA. While COX-2 and mPGES-1 expression was significantly upregulated by AGEs, COX-1 and cPGES expression was not affected by AGE. AGE-stimulated COX-2 and mPGES-1 expression was attenuated by HA through CD44 (HA receptor). However, the changes in COX-1 and cPGES expression were almost negligible. Conclusion: In meniscal cells from osteoarthritic knees, AGEs increased the production of inflammatory mediators, including PGE2, COX-2 and mPGES-1. Furthermore, HA could decrease AGE-induced production of PGE2, COX-2 and mPGES-1 through CD44.</subfield>
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   <subfield code="a">Springer Basel AG, 2011</subfield>
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   <subfield code="a">Advanced glycation end products</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Meniscal cell</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Osteoarthritis</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Inflammatory mediator</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hyaluronan</subfield>
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   <subfield code="a">AGEs : Advanced glycation end-products</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">BSA : Bovine serum albumin</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">RAGE : The receptor for advanced glycation end products</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">OA : Osteoarthritis</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">HA : Hyaluronan</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">PGE2 : Prostaglandin E2</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">COX : Cyclooxygenase</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">mPGES : Membrane associated prostaglandin E synthase</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">cPGES : Cytosolic prostaglandin E synthase</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Hiraiwa</subfield>
   <subfield code="D">Hideki</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Sakai</subfield>
   <subfield code="D">Tadahiro</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Mitsuyama</subfield>
   <subfield code="D">Hirohito</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
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   <subfield code="a">Hamada</subfield>
   <subfield code="D">Takashi</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Yamamoto</subfield>
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   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
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   <subfield code="a">Omachi</subfield>
   <subfield code="D">Takaaki</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
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   <subfield code="a">Ohno</subfield>
   <subfield code="D">Yohei</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
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   <subfield code="a">Nakashima</subfield>
   <subfield code="D">Motoshige</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
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   <subfield code="a">Ishiguro</subfield>
   <subfield code="D">Naoki</subfield>
   <subfield code="u">Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan</subfield>
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   <subfield code="g">60/11(2011-11-01), 1039-1048</subfield>
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