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首页> 外文期刊>Rheumatology >IL-6-accelerated calcification by induction of ROR2 in human adipose tissue-derived mesenchymal stem cells is STAT3 dependent
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IL-6-accelerated calcification by induction of ROR2 in human adipose tissue-derived mesenchymal stem cells is STAT3 dependent

机译：在人脂肪组织间充质干细胞中诱导ROR2引起的IL-6加速钙化是STAT3依赖性的

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Objective: The mechanisms of ectopic calcification in inflammatory diseases are poorly understood. We investigated the effects of inflammatory cytokines on the mechanisms of calcification in human adipose tissue-derived mesenchymal stem cells (hADSCs). Methods: The effects of inflammatory cytokines were evaluated using hADSCs cultured in osteoblast induction medium. mRNA expression was measured by real-time PCR and protein levels were measured by western blotting. Cell mineralization was evaluated by Alizarin Red S staining. Results: In hADSCs, administration of IL-6/soluble IL-6 receptor (sIL-6R), TNF or IL-1b accelerated calcification through enhanced expression of an osteoblast differentiation marker, runt-related transcription factor 2 (RUNX2). IL-6/sIL-6R had the greatest effect. The transcription of mRNA for receptor tyrosine kinase-like orphan receptor 2 (ROR2), involved in the non-canonical wingless-type (WNT) MMTV integration site pathway, was increased, while b-catenin expression, an essential factor in the canonical WNT signalling pathway for osteoblast differentiation, did not change. Suppression of signal transducer and activator of transcription 3 (STAT3), but not STAT1, by small interfering RNA (siRNA) exerted a strong inhibitory effect on RUNX2 and ROR2 expression, and inhibited accelerated calcification. Conclusion: IL-6/sIL-6R stimulation accelerated the ROR2/WNT5A pathway in hADSCs in a STAT3- dependent manner, resulting in augmented calcification. These results suggest that the mechanisms of ectopic calcification accelerated by IL-6 in hADSCs may be involved in chronic inflammatory tissues and that IL-6 inhibitors may be beneficial in the treatment of ectopic calcification in inflammatory diseases.
机译：目的：对炎症疾病中异位钙化的机制了解甚少。我们研究了炎症细胞因子对人脂肪组织间充质干细胞（hADSCs）钙化机制的影响。方法：使用在成骨细胞诱导培养基中培养的hADSCs评估炎症细胞因子的作用。通过实时PCR测量mRNA表达，并通过蛋白质印迹法测量蛋白质水平。通过茜素红S染色评估细胞矿化。结果：在hADSCs中，通过增强成骨细胞分化标记物，矮子相关转录因子2（RUNX2）的表达，给予IL-6 /可溶性IL-6受体（sIL-6R），TNF或IL-1b可以加速钙化。 IL-6 / sIL-6R影响最大。参与非经典无翼型（WNT）MMTV整合位点通路的受体酪氨酸激酶样孤儿受体2（ROR2）的mRNA转录增加，而b-catenin表达是经典WNT的重要因素。成骨细胞分化的信号通路没有改变。通过小的干扰RNA（siRNA）抑制信号转导和转录激活因子3（STAT3），但不抑制STAT1，对RUNX2和ROR2表达产生强烈的抑制作用，并抑制加速钙化。结论：IL-6 / sIL-6R刺激以STAT3依赖性方式加速了hADSCs中的ROR2 / WNT5A途径，导致钙化增强。这些结果表明，hADSCs中由IL-6促进的异位钙化机制可能与慢性炎症组织有关，并且IL-6抑制剂可能对治疗炎性疾病中的异位钙化有益。

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