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.
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 humanosteoarthritic 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.
Authors: A Taguchi; D C Blood; G del Toro; A Canet; D C Lee; W Qu; N Tanji; Y Lu; E Lalla; C Fu; M A Hofmann; T Kislinger; M Ingram; A Lu; H Tanaka; O Hori; S Ogawa; D M Stern; A M Schmidt Journal: Nature Date: 2000-05-18 Impact factor: 49.962
Authors: Richard F Loeser; Raghunatha R Yammani; Cathy S Carlson; Hong Chen; Ada Cole; Hee-Jeong Im; Laura S Bursch; Shi Du Yan Journal: Arthritis Rheum Date: 2005-08
Authors: Marjan M C Steenvoorden; Tom W J Huizinga; Nicole Verzijl; Ruud A Bank; H Karel Ronday; Hilco A F Luning; Floris P J G Lafeber; René E M Toes; Jeroen DeGroot Journal: Arthritis Rheum Date: 2006-01
Authors: Angela Avenoso; Angela D'Ascola; Michele Scuruchi; Giuseppe Mandraffino; Alberto Calatroni; Antonino Saitta; Salvatore Campo; Giuseppe M Campo Journal: Inflamm Res Date: 2017-08-12 Impact factor: 4.575