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【medical-news】MAPK-APK2是调控与骨性关节炎病理相
Osteoarthritis and Cartilage
Objective
To examine the role of mitogen-activated protein kinase-activated protein kinase 2 (MK2) in mediating the cellular response to pro-inflammatory cytokines in human primary osteoarthritis (OA) chondrocytes.
Methods
Delivery of a dominant negative MK2 was achieved in HeLa cells by adenoviral infection. Cellular heat shock protein (HSP27) activity was determined using a Bioplex assay. Primary OA chondrocytes were isolated by collagenase digestion of human articular cartilage. Phosphorylated MK2 was detected by immunoblotting and immunohistology. Transfection of primary chondrocytes with siRNA was achieved using cationic lipid and gene expression determined by real-time polymerase chain reaction. Production of prostaglandin E2 (PGE2) and matrixmetalloproteases (MMPs) was measured by enzyme-linked immunosorbent assay.
Results
Over-expression of a dominant negative MK2 inhibited HSP27 phosphorylation and significantly reduced both interleukin 1 (IL-1)β and tumour necrosis factor (TNF)-α mediated release of PGE2 in HeLa cells over a 24 h period. Phosphorylated MK2 was detected in OA articular cartilage and in isolated primary OA chondrocytes, where it was induced by IL-1β. Transfection of OA chondrocytes with MK2 siRNA antisense significantly reduced both basal and IL-1β induced PGE2 release. siRNA mediated MK2 knockdown also significantly reduced both basal and IL-1β induced MMP13 expression and MMP13 and MMP3 protein release but had no effect on MMP1.
Conclusions
Our data reveal that MK2 is active in OA human articular cartilage and in isolated primary human chondrocytes and that MK2 mediates the release of PGE2, MMP3 and MMP13. These findings suggest a role for MK2 in contributing to OA algesia and OA joint structural deterioration by mediating the downstream effects of p38 activation on PGE2 release and the expression and release of catabolic proteases.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WP3-4SSGCRK-1&_user=10&_coverDate=06%2F17%2F2008&_rdoc=21&_fmt=high&_orig=browse&_srch=doc-info(%23toc%236979%239999%23999999999%2399999%23FLA%23display%23Articles)&_cdi=6979&_sort=d&_docanchor=&_ct=107&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=02452ee8c68a8e6af98e5af71d0fbd45 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。
第一次翻译，试着做一下，恳请大家批评指正 学习了,不过好象需要进一步的验证 Mitogen-activated protein kinase-activated protein kinase 2 (MK2) modulates key biological pathways associated with OA disease pathology
Osteoarthritis and Cartilage
有丝分裂原激活蛋白激酶活化蛋白激酶2 （ MK2 ）调制主要生物学途径与办公自动化系统疾病的病理
骨性关节炎和关节软骨
Objective
To examine the role of mitogen-activated protein kinase-activated protein kinase 2 (MK2) in mediating the cellular response to pro-inflammatory cytokines in human primary osteoarthritis (OA) chondrocytes
目的
检查的作用，有丝分裂原激活蛋白激酶活化蛋白激酶2 （ MK2 ）在调解的细胞反应前炎症细胞因子在人类初级骨关节炎（ OA ）软骨细胞
Methods
Delivery of a dominant negative MK2 was achieved in HeLa cells by adenoviral infection. Cellular heat shock protein (HSP27) activity was determined using a Bioplex assay. Primary OA chondrocytes were isolated by collagenase digestion of human articular cartilage. Phosphorylated MK2 was detected by immunoblotting and immunohistology. Transfection of primary chondrocytes with siRNA was achieved using cationic lipid and gene expression determined by real-time polymerase chain reaction. Production of prostaglandin E2 (PGE2) and matrixmetalloproteases (MMPs) was measured by enzyme-linked immunosorbent assay.
方法
交付显性负MK2取得了在HeLa细胞中腺病毒感染。蜂窝热休克蛋白（热休克蛋白27 ）的活性测定使用Bioplex检测。原发性骨关节炎软骨细胞分离胶原酶消化人类关节软骨。 MK2磷酸化检测免疫印迹和免疫组织化学。转初级软骨细胞与小分子干扰核糖核酸取得使用阳离子脂质和基因表达取决于实时聚合酶链反应。生产中的前列腺素E2 （ PGE2的）和matrixmetalloproteases蛋白酶（ MMPs ）是衡量酶联免疫吸附试验。
检查的作用，有丝分裂原激活蛋白激酶活化蛋白激酶2 （ MK2 ）在调解的细胞反应前炎症细胞因子在人类初级骨关节炎（ OA ）软骨细胞
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作者:admin@医学,生命科学 2010-10-23 17:11
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