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The effects of interleukin-1β in modulating osteoclast-conditioned medium's influence on gelatinases in chondrocytes through mitogen-activated protein kinases
by
Jing Xie Na Fu Lin-Yi Cai Tao Gong Guo Li Qiang Peng Xiao-Xiao Cai
in
IL-1β
/ 丝裂原活化蛋白激酶
/ 明胶酶
/ 条件培养基
/ 白细胞介素-1β
/ 破骨细胞
/ 细胞外信号调节激酶
/ 软骨细胞
2015
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The effects of interleukin-1β in modulating osteoclast-conditioned medium's influence on gelatinases in chondrocytes through mitogen-activated protein kinases
by
Jing Xie Na Fu Lin-Yi Cai Tao Gong Guo Li Qiang Peng Xiao-Xiao Cai
in
IL-1β
/ 丝裂原活化蛋白激酶
/ 明胶酶
/ 条件培养基
/ 白细胞介素-1β
/ 破骨细胞
/ 细胞外信号调节激酶
/ 软骨细胞
2015
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The effects of interleukin-1β in modulating osteoclast-conditioned medium's influence on gelatinases in chondrocytes through mitogen-activated protein kinases
by
Jing Xie Na Fu Lin-Yi Cai Tao Gong Guo Li Qiang Peng Xiao-Xiao Cai
in
IL-1β
/ 丝裂原活化蛋白激酶
/ 明胶酶
/ 条件培养基
/ 白细胞介素-1β
/ 破骨细胞
/ 细胞外信号调节激酶
/ 软骨细胞
2015
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The effects of interleukin-1β in modulating osteoclast-conditioned medium's influence on gelatinases in chondrocytes through mitogen-activated protein kinases
Journal Article
The effects of interleukin-1β in modulating osteoclast-conditioned medium's influence on gelatinases in chondrocytes through mitogen-activated protein kinases
2015
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Overview
Osteoarthritis is recognised to be an interactive pathological process involving the cartilage, subchondral bone and synovium. The signals from the synovium play an important role in cartilage metabolism, but little is known regarding the influence of the signalling from bone. Additionally, the collagenases and stromelysin-1 are involved in cartilage catabolism through mitogen-activated protein kinase (MAPK) signalling, but the role of the gelatinases has not been elucidated. Here, we studied the influence of osteoclastic signals on chondrocytes by characterising the expression of interleukin-1β (IL-1β)-induced gelatinases through MAPK signalling. We found that osteoclast-conditioned media attenuated the gelatinase activity in chondrocytes. However, IL-1β induced increased levels of gelatinase activity in the conditioned media group relative to the mono-cultured chondrocyte group. More specifically, IL-1β restored high levels of gelatinase activity in c-Jun N-terminal kinase inhibitor-pretreated chondrocytes in the conditioned media group and led to lower levels of gelatinase activity in extracellular signal-regulated kinase or p38 inhibitor-pretreated chondrocytes. Gene expression generally correlated with protein expression. Taken together, these results show for the first time that signals from osteoclasts can influence gelatinase activity in chondrocytes. Furthermore, these data show that IL-11~ restores gelatinase activity through MAPK inhibitors; this information can help to increase the understanding of the gelatinase modulation in articular cartilage.
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