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Inflamm Res. 2011 Nov;60(11):1039-48. doi: 10.1007/s00011-011-0365-y. Epub 2011 Aug 13.

Inflammatory effect of advanced glycation end products on human meniscal cells from osteoarthritic knees.

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Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan.



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.


Meniscal cells from human osteoarthritic knees were cultured with or without glycolaldehyde-AGE-bovine serum albumin and 800 kDa HA. The amount of prostaglandin E(2) (PGE(2)) 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.


PGE(2) synthesis was significantly increased by AGEs, and AGE-induced PGE(2) 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.


In meniscal cells from osteoarthritic knees, AGEs increased the production of inflammatory mediators, including PGE(2), COX-2 and mPGES-1. Furthermore, HA could decrease AGE-induced production of PGE(2), COX-2 and mPGES-1 through CD44.

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