Mingcheng Huang1, Lihui Wang2, Shan Zeng1, Qian Qiu1, Yaoyao Zou1, Maohua Shi1, Hanshi Xu1, Liuqin Liang3. 1. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, Guangdong, China. 2. Department of Orthopedics, The People's Hospital of Nanhai District, Foshan, Guangdong, China. 3. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, Guangdong, China. lliuq@mail.sysu.edu.cn.
Abstract
OBJECTIVES: To evaluate the inhibition of indirubin in FLSs migration, invasion, activation, and proliferation in RA FLSs. METHODS: The levels of IL-6 and IL-8 in cultural supernatants were measured by ELISA. RA FLS migration and invasion in vitro were measured by the Boyden chamber method and the scratch assay. Signal transduction protein expression was measured by western blot. FLS proliferation was detected by Edu incorporation. F-actin was measured by immunofluorescence staining. RESULTS: We found that indirubin reduced migration, invasion, inflammation, and proliferation in RA FLSs. In addition, we demonstrated that indirubin inhibited lamellipodium formation during cell migration. To gain insight into molecular mechanisms, we evaluated the effect of indirubin on PAK1 and MAPK activation. Our results indicated that indirubin inhibited the activity of PAK1 and MAPK. CONCLUSIONS: Our observations suggest that indirubin may be protective against joint destruction in RA by regulating synoviocyte migration, invasion, activation, and proliferation.
OBJECTIVES: To evaluate the inhibition of indirubin in FLSs migration, invasion, activation, and proliferation in RA FLSs. METHODS: The levels of IL-6 and IL-8 in cultural supernatants were measured by ELISA. RA FLS migration and invasion in vitro were measured by the Boyden chamber method and the scratch assay. Signal transduction protein expression was measured by western blot. FLS proliferation was detected by Edu incorporation. F-actin was measured by immunofluorescence staining. RESULTS: We found that indirubin reduced migration, invasion, inflammation, and proliferation in RA FLSs. In addition, we demonstrated that indirubin inhibited lamellipodium formation during cell migration. To gain insight into molecular mechanisms, we evaluated the effect of indirubin on PAK1 and MAPK activation. Our results indicated that indirubin inhibited the activity of PAK1 and MAPK. CONCLUSIONS: Our observations suggest that indirubin may be protective against joint destruction in RA by regulating synoviocyte migration, invasion, activation, and proliferation.
Authors: R Hoessel; S Leclerc; J A Endicott; M E Nobel; A Lawrie; P Tunnah; M Leost; E Damiens; D Marie; D Marko; E Niederberger; W Tang; G Eisenbrand; L Meijer Journal: Nat Cell Biol Date: 1999-05 Impact factor: 28.824
Authors: J Ribas; K Bettayeb; Y Ferandin; M Knockaert; X Garrofé-Ochoa; F Totzke; C Schächtele; J Mester; P Polychronopoulos; P Magiatis; A-L Skaltsounis; J Boix; L Meijer Journal: Oncogene Date: 2006-05-15 Impact factor: 9.867