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首页> 外文期刊>Journal of cellular physiology. >Zika virus alters osteogenic lineage progression of human mesenchymal stromal cells
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Zika virus alters osteogenic lineage progression of human mesenchymal stromal cells

机译：寨卡病毒改变人间充质基质细胞的成骨谱系进展

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Abstract Arboviruses target bone forming osteoblasts and perturb bone remodeling via paracrine factors. We previously reported that Zika virus (ZIKV) infection of early‐stage human mesenchymal stromal cells (MSCs) inhibited the osteogenic lineage commitment of MSCs. To understand the physiological interplay between bone development and ZIKV pathogenesis, we employed a primary in vitro model to examine the biological responses of MSCs to ZIKV infection at different stages of osteogenesis. Precommitted MSCs were infected at the late stage of osteogenic stimulation (Day 7) with ZIKV (multiplicity of infection?of 5). We observe that MSCs infected at the late stage of differentiation are highly susceptible to ZIKV infection similar to previous observations with early stage infected MSCs (Day 0). However, in contrast to ZIKV infection at the early stage of differentiation, infection at a later stage significantly elevates the key osteogenic markers and calcium content. Comparative RNA sequencing (RNA‐seq) of early and late stage infected MSCs reveals that ZIKV infection alters the mRNA transcriptome during osteogenic induction of MSCs (1251 genes). ZIKV infection provokes a robust antiviral response at both stages of osteogenic differentiation as reflected by the upregulation of interferon responsive genes (n?>?140). ZIKV infection enhances the expression of immune‐related genes in early stage MSCs while increasing cell cycle genes in late stage MSCs. Remarkably, ZIKA infection in early stage MSCs also activates lipid metabolism‐related pathways. In conclusion, ZIKV infection has differentiation stage‐dependent effects on MSCs and this mechanistic understanding may permit the development of new therapeutic or preventative measures for bone‐related effects of ZIKV infection.
机译：抽象的虫媒病毒的目标骨形成成骨细胞和扰乱骨重塑通过旁分泌的因素。Zika病毒(ZIKV)感染的早期人类的必经阶段间充质基质细胞(msc)抑制了成骨的血统msc的承诺。了解生理相互作用骨骼发育和ZIKV发病机理,我们检查工作主要在体外模型骨髓间充质ZIKV感染的生物反应不同的骨生成阶段。后期的msc被感染与ZIKV成骨的刺激(7天)(感染复数?msc感染的后期阶段分化对ZIKV高度敏感感染类似于以前的观测早期感染msc(第0天)。然而,对比ZIKV感染的早期阶段在稍后阶段分化、感染显著提升的关键成骨的标记和钙含量。(RNA必经seq)的早期和晚期感染的msc表明ZIKV感染改变了信使rna转录组在成骨诱导msc(1251个基因)。成骨的抗病毒反应在两个阶段分化upregulation反映的干扰素反应基因(n > ? 140)。感染增强的表现免疫相关基因在早期msc增加细胞周期基因后期msc。值得注意的是,ZIKA病毒感染早期msc也激活了脂质代谢相关的通路。总之,ZIKV感染分化对msc和这个阶段还是依赖的影响机械的理解可能会允许开发新的治疗或预防ZIKV相关措施对骨骼的影响感染。

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