Semaphorin 3A Inhibits Inflammation in Chondrocytes under Excessive Mechanical Stress.
Semaphorin 3A Inhibits Inflammation in Chondrocytes under Excessive Mechanical Stress.
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DOI：
10.1155/2018/5703651
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发表时间：
2018
影响因子：
4.6
通讯作者：
Tanimoto K
中科院分区：
文献类型：
--
作者：
Sumi C;Hirose N;Yanoshita M;Takano M;Nishiyama S;Okamoto Y;Asakawa Y;Tanimoto K
过度的机械应力导致软骨炎症和破坏，被认为是骨关节炎（OA）的原因之一。信号蛋白3A （Sema3A）是一种轴突引导分子，已被证实在软骨细胞中表达。然而，关于Sema3A在软骨细胞中的作用的报道很少，Sema3A对软骨炎症的影响也知之甚少。本研究的目的是研究Sema3A在高强度循环拉伸应变（CTS）引起的炎症中的作用。Western blot检测Sema3A及其受体neuropilin-1 （NRP-1）和plexin-A1 （PLXA1）在ATDC5细胞中的表达。ATDC5细胞接受0.5 Hz， 10%延伸率的CTS，添加Sema3A 3小时。采用qPCR检测IL-1β、TNF- β、COX-2、MMP-3、MMP-13的基因表达。Western blot检测AKT、ERK、NF-κB的磷酸化水平。添加Sema3A抑制CTS上调的炎性细胞因子基因表达呈剂量依赖性。Sema3A的加入以剂量依赖性的方式抑制AKT、ERK和NF-κB的激活。Sema3A通过下调ATDC5细胞中AKT、ERK和NF-κB通路的激活，降低炎症细胞因子的基因表达。
Excessive mechanical stress causes inflammation and destruction of cartilage and is considered one of the cause of osteoarthritis (OA). Expression of semaphorin 3A (Sema3A), which is an axon guidance molecule, has been confirmed in chondrocytes. However, there are few reports about Sema3A in chondrocytes, and the effects of Sema3A on inflammation in the cartilage are poorly understood. The aim of this study was to examine the role of Sema3A in inflammation caused by high magnitude cyclic tensile strain (CTS). Expression of Sema3A and its receptors neuropilin-1 (NRP-1) and plexin-A1 (PLXA1) in ATDC5 cells was examined by Western blot analysis. ATDC5 cells were subjected to CTS of 0.5 Hz, 10% elongation with added Sema3A for 3 h. Gene expression of IL-1β, TNF-ɑ, COX-2, MMP-3, and MMP-13 was examined by qPCR analysis. Furthermore, the phosphorylation of AKT, ERK, and NF-κB was detected by Western blot analysis. Added Sema3A inhibited the gene expression of inflammatory cytokines upregulated by CTS in a dose-dependent manner. Addition of Sema3A suppressed the activation of AKT, ERK, and NF-κB in a dose-dependent manner. Sema3A reduces the gene expression of inflammatory cytokines by downregulating the activation of AKT, ERK, and NF-κB pathways in ATDC5 cells under CTS.
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DOI：
10.1016/j.bbapap.2005.08.017
发表时间：
2005-12-30
影响因子：
3.2
作者：
Kaminska, B
通讯作者：
Kaminska, B
DOI：
10.1016/0922-3371(90)90079-c
发表时间：
1990-05-01
期刊：
CELL DIFFERENTIATION AND DEVELOPMENT
影响因子：
--
作者：
ATSUMI, T;MIWA, Y;IKAWA, Y
通讯作者：
IKAWA, Y
影响因子：
6.2
作者：
Longobardi, L;O'Rear, L;Spagnoli, A
通讯作者：
Spagnoli, A
影响因子：
6.6
作者：
Honda, K;Ohno, S;Tanne, K
通讯作者：
Tanne, K
影响因子：
3.9
作者：
Staton, Carolyn A.
通讯作者：
Staton, Carolyn A.