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首页> 外文期刊>Osteoarthritis and cartilage >Roles for the interleukin-4 receptor and associated JAK/STAT proteins in human articular chondrocyte mechanotransduction.
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Roles for the interleukin-4 receptor and associated JAK/STAT proteins in human articular chondrocyte mechanotransduction.

机译：白细胞介素4受体和相关的JAK / STAT蛋白在人关节软骨细胞机械转导中的作用。

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OBJECTIVE: To identify functional interleukin-4 (IL4) receptor (IL4R) subtypes and associated Janus kinase/signal transducers and activators of transcription (JAK/STAT) molecules in human articular chondrocytes and assess the role of JAK/STAT proteins in chondrocyte mechanotransduction. METHODS: Expression of IL4R subunits and associated molecules was assessed by immunohistochemistry and western blotting. Functional IL4R were identified by chemical crosslinking of IL4-stimulated chondrocytes and western blotting. JAK and STAT phosphorylation was assessed by western blotting. RESULTS: Chondrocytes from normal and osteoarthritic (OA) cartilage express IL4Ralpha, gammac and IL13Ralpha1 subunits (components of the Type I and Type II IL4R). In the presence of IL4 only functional Type II IL4Rs were identified in normal or OA chondrocytes. With the exception of STAT2, no differences in JAK/STAT expression were detected between normal and OA cartilage. STAT2 was expressed in OA but not normal chondrocytes. Mechanical stimulation (MS) resulted in an IL4R-dependent increase in phosphorylated Tyk2 in normal chondrocytes, which could be abolished by IL1beta preincubation. No phosphorylation of STAT5 or STAT6 was detected in either normal or OA chondrocytes following mechanical stimulation (MS) IL4 stimulation resulted in a decrease in Tyk2 phosphorylation and an increase in phosphorylation of STAT6 in both normal and OA chondrocytes. CONCLUSION: Chondrocytes from normal and OA cartilage signal through a Type II IL4R. This signalling is via a STAT6-independent pathway. Differences in IL4 signalling are likely due to crosstalk between integrin and cytokine signalling pathways, and not differences in IL4R expression.
机译：目的：鉴定人关节软骨细胞中功能性白介素4（IL4）受体（IL4R）亚型以及相关的Janus激酶/信号转导子和转录激活因子（JAK / STAT）分子，并评估JAK / STAT蛋白在软骨细胞机械转导中的作用。方法：通过免疫组织化学和蛋白质印迹法评估IL4R亚基和相关分子的表达。通过IL4刺激的软骨细胞的化学交联和蛋白质印迹来鉴定功能性IL4R。通过蛋白质印迹评估JAK和STAT的磷酸化。结果：来自正常和骨关节炎（OA）软骨的软骨细胞表达IL4Ralpha，gammac和IL13Ralpha1亚基（I型和II型IL4R的组成部分）。在存在IL4的情况下，在正常或OA软骨细胞中仅鉴定出功能性II型IL4R。除了STAT2，在正常和OA软骨之间未检测到JAK / STAT表达的差异。 STAT2在OA中表达，但在正常软骨细胞中不表达。机械刺激（MS）导致正常软骨细胞磷酸化Tyk2依赖IL4R的增加，这可以通过IL1beta预温育来消除。机械刺激（MS）后，在正常或OA软骨细胞中均未检测到STAT5或STAT6的磷酸化。IL4刺激导致正常和OA软骨细胞中Tyk2磷酸化的降低和STAT6磷酸化的增加。结论：来自正常和OA软骨信号的软骨细胞通过II型IL4R。该信号传导是通过STAT6非依赖性途径。 IL4信号的差异很可能是由于整联蛋白和细胞因子信号通路之间的串扰引起的，而不是IL4R表达的差异。

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