Related Experiment Video
Updated: May 30, 2026
Glycemic Impact on Knee Osteoarthritis Symptoms on Physical, Radiographic, and Inflammatory Markers among Individuals Aged 50 and Over with Diabetes
Published on: March 7, 2025
Inflammatory effect of advanced glycation end products on human meniscal cells from osteoarthritic knees
Hideki Hiraiwa1, Tadahiro Sakai, Hirohito Mitsuyama
1Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan. hirahide@med.nagoya-u.ac.jp
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 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.
Results:
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.
Conclusion:
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.
