Transcriptome analysis of the mandibles from FcgRIIB-deficient mouse model of lupus

To identify the extensive complexity of transcriptome in Fc gamma receptor IIB knockout (FcgRIIB-/-) mandibles. We performed gene expression profiling of mandibular bone from wild-type (WT) and FcgRIIB-/- mice at 6 months of age. Our study reports the first transcriptomic analysis in mandibles of FcgRIIB-deficient mice using RNA-sequencing (RNA-seq). The data were validated by qPCR analysis. qPCR analysis revealed similar results compared to RNA-seq data. This finding disclosed the relevant differentially expressed genes (DEGs) and clarify the mechanism underlying the pathogenesis of osteopenia. We provide novel candidate genes and enriched pathways that contribute to mandibular bone loss in FcgRIIB-/- mice during lupus development. Sufu and Serpina12 were identified as candidate molecular targets regulating osteoclastogenesis and osteogenesis, respectively. Mandibular transcriptional profiles of 6-month-old WT controls and FcgRIIB-/- male mice本研究旨在解析Fcγ受体IIB敲除（Fc gamma receptor IIB knockout, FcγRIIB-/-）小鼠下颌骨转录组的复杂全貌。我们对6月龄野生型（wild-type, WT）与FcγRIIB-/-小鼠的下颌骨组织开展了基因表达谱分析。本研究首次利用RNA测序（RNA-sequencing, RNA-seq）技术，对FcγRIIB缺陷小鼠的下颌骨进行转录组学分析。我们通过定量聚合酶链反应（quantitative PCR, qPCR）分析对测序数据进行了验证，且qPCR结果与RNA-seq数据高度吻合。该研究明确了与骨质减少发病机制相关的差异表达基因（differentially expressed genes, DEGs），并阐明了其潜在作用机制。本研究筛选出了在狼疮病程中参与FcγRIIB-/-小鼠下颌骨骨丢失的新型候选基因及富集通路。研究鉴定出Sufu和Serpina12分别作为调控破骨细胞生成（osteoclastogenesis）与成骨细胞生成（osteogenesis）的候选分子靶点。本数据集涵盖6月龄野生型对照及FcγRIIB-/-雄性小鼠的下颌骨转录组图谱。