Dataset related to article "Genetic Deficiency of the Long Pentraxin 3 Affects Osteogenesis and Osteoclastogenesis in Homeostatic and Inflammatory Conditions "

This record contains raw data related to article “Genetic Deficiency of the Long Pentraxin 3 Affects Osteogenesis and Osteoclastogenesis in Homeostatic and Inflammatory Conditions" Abstract The long pentraxin 3 (PTX3) is a soluble glycoprotein made by immune and nonimmune cells endowed with pleiotropic functions in innate immunity, inflammation, and tissue remodeling. PTX3 has recently emerged as a mediator of bone turnover in both physiological and pathological conditions, with direct and indirect effects on osteoblasts and osteoclasts. This notwithstanding, its role in bone biology, with major regard to the osteogenic potential of osteoblasts and their interplay with osteoclasts, is at present unclear. Here, we investigated the contribution of this pentraxin to bone deposition in the osteogenic lineage by assessing collagen production, mineralization capacity, osteoblast maturation, extracellular matrix gene expression, and inflammatory mediators' production in primary osteoblasts from the calvaria of wild-type (WT) and Ptx3-deficient (Ptx3-/-) mice. Also, we evaluated the effect of PTX3 on osteoclastogenesis in cocultures of primary osteoblasts and bone marrow-derived osteoclasts. Our investigations were carried out both in physiological and inflammatory conditions to recapitulate in vitro aspects of inflammatory diseases of the bone. We found that primary osteoblasts from WT animals constitutively expressed low levels of the protein in osteogenic noninflammatory conditions, and genetic ablation of PTX3 in these cells had no major impact on collagen and hydroxyapatite deposition. However, Ptx3-/- osteoblasts had an increased RANKL/OPG ratio and CD44 expression, which resulted in in enhanced osteoclastogenesis when cocultured with bone marrow monocytes. Inflammation (modelled through administration of tumor necrosis factor-α, TNF-α) boosted the expression and accumulation of PTX3 and inflammatory mediators in WT osteoblasts. In these conditions, Ptx3 genetic depletion was associated with reduced collagen deposition and immune modulators' production. Our study shed light on the role of PTX3 in osteoblast and osteoclast biology and identified a major effect of inflammation on the bone-related properties of this pentraxin, which might be relevant for therapeutic and/or diagnostic purposes in musculoskeletal pathology.本数据集包含与论文《长五聚蛋白3（Long Pentraxin 3, PTX3）基因缺陷影响稳态与炎症状态下的成骨与破骨细胞生成》相关的原始数据。 摘要 长五聚蛋白3（Long Pentraxin 3, PTX3）是一种由免疫细胞与非免疫细胞分泌的可溶性糖蛋白，在先天免疫、炎症反应及组织重塑中具有多效性功能。近期研究表明，PTX3可作为骨代谢的介导因子参与生理与病理状态下的骨稳态调控，对成骨细胞与破骨细胞存在直接与间接调控作用。尽管如此，目前其在骨生物学中的作用仍不明确，尤其是针对成骨细胞的成骨潜能及其与破骨细胞的相互作用机制。 本研究通过检测野生型（wild-type, WT）与Ptx3基因缺陷型（Ptx3-/-）小鼠颅骨原代成骨细胞的胶原生成能力、矿化潜能、成骨细胞成熟度、细胞外基质基因表达及炎症介质分泌情况，探究了该五聚蛋白在成骨细胞谱系骨沉积中的作用。此外，我们通过原代成骨细胞与骨髓来源破骨细胞的共培养体系，评估了PTX3对破骨细胞生成的影响。本研究在生理与炎症两种状态下开展实验，以复现骨骼炎症性疾病的体外特征。 研究结果显示：在成骨非炎症状态下，野生型动物的原代成骨细胞仅基础表达低水平的PTX3，且PTX3基因敲除对该状态下的胶原与羟磷灰石沉积无显著影响；但Ptx3-/-成骨细胞的RANKL/OPG比值与CD44表达水平升高，当其与骨髓单核细胞共培养时，可诱导更强的破骨细胞生成。炎症状态（通过肿瘤坏死因子-α（tumor necrosis factor-α, TNF-α）造模）可促进野生型成骨细胞中PTX3与炎症介质的表达与积累；在此状态下，Ptx3基因缺陷会导致胶原沉积与免疫调节因子分泌水平下降。 本研究阐明了PTX3在成骨细胞与破骨细胞生物学中的作用，并揭示了炎症对该五聚蛋白骨相关功能的显著调控效应，这一发现或许可为肌肉骨骼疾病的治疗与诊断提供新的参考价值。