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首页> 外文期刊>Journal of Cellular Physiology >Connective tissue growth factor (CTGF) acts as a downstream mediator of TGF-beta1 to induce mesenchymal cell condensation.
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Connective tissue growth factor (CTGF) acts as a downstream mediator of TGF-beta1 to induce mesenchymal cell condensation.

机译：结缔组织生长因子(CTGF)充当下游TGF-beta1诱导的中介间充质细胞的凝结。

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摘要

Mesenchymal cell (MC) condensation or the aggregation of MCs precedes chondrocyte differentiation and is required for subsequent cartilage formation during endochondral ossification. In this study, we used micromass cultures of C3H10T1/2 cells as an in vitro model system for studying MC condensation and the events important for this process. Transforming growth factor beta1 (TGF-beta1) served as the initiator of MC condensation in our model system and we were interested in determining whether CTGF functions as a downstream mediator of TGF-beta1. CTGF is a matricellular protein that has been found to be expressed in MC condensations and in the perichondrium. Micromass cultures of C3H10T1/2 cells condensed under TGF-beta1 stimulation concomitant with dramatic up-regulation of CTGF mRNA and protein levels. CTGF silencing by either CTGF siRNA or CTGF antisense oligonucleotide approaches showed that TGF-beta1-induced condensation was CTGF dependent. Furthermore, silencing of CTGF expression resulted in significant reductions in cell proliferation and migration, events that are crucial during MC condensation. In addition, up-regulation of Fibronectin (FN) and suppression of Sox9 expression by TGF-beta1 was also found to be mediated by CTGF. Immunofluorescence of developing mouse vertebrae showed that CTGF, TGF-beta1 and FN were co-expressed in condensations of MCs, while Sox9 expression was low at this stage. During subsequent chondrogenesis, Sox9 expression was high in chondrocytes while CTGF expression was limited to the perichondrium. Thus, CTGF is an essential downstream mediator of TGF-beta1-induced MC condensation through its effects on cell proliferation and migration. CTGF is also involved in up-regulating FN and suppressing Sox9 expression during TGF-beta1 induced MC condensation.
机译：间充质细胞(MC)凝结或聚合的MCs先于软骨细胞分化和随后的需要软骨形成在软骨内骨化。文化C3H10T1/2细胞作为体外模型系统研究MC冷凝物和事件重要的这一过程。生长因子beta1 (TGF-beta1)担任发起人的MC凝结在我们的模型系统我们决定是否感兴趣CTGF的下游中介功能TGF-beta1。被发现在MC表达吗冷凝和软骨膜。文化C3H10T1/2细胞凝聚TGF-beta1刺激相伴与戏剧性老年病CTGF信使rna和蛋白质的水平。由CTGF siRNA或CTGF CTGF沉默反义寡核苷酸的方法显示TGF-beta1-induced凝结是CTGF相关的。表达导致显著减少细胞增殖和迁移,事件在MC凝结至关重要。老年病的纤连蛋白(FN)和抑制的表达Sox9 TGF-beta1也发现是由CTGF。发展中鼠标椎骨显示CTGF,TGF-beta1和FN中的MCs的冷凝,而表达Sox9在这个阶段。软骨形成、Sox9表达式是高的软骨细胞虽然仅限于CTGF表达软骨膜。下游TGF-beta1-induced MC的中介冷凝通过其对细胞的影响增殖和迁移。参与调控的FN和抑制Sox9表达在TGF-beta1诱导MC凝结。

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