Osteoporosis is the most common degenerative bone disease that occurs when the balance of bone production and resorption is perturbed. Loss of bone mass or alteration in its quality leads to significant weakening of the bones and subsequently to higher fracture risk. Collagen XIII (ColXIII) is a conserved transmembrane protein expressed in many mesenchymal tissues. Here we show that ColXIII is a regulator of bone remodeling niche. In this study, we found that ColXIII expression is significantly upregulated in osteoporotic patients. In view of that, we studied bone homeostasis in ColXIII-overexpressing mice (Col13a1oe) up to 72 weeks of age and observed a cortical bone overgrowth followed by a drastic bone loss, together with increased bone vascularization. Moreover, our results demonstrate that the ColXIII-derived ectodomain enhances angiogenesis through β1-integrins and the JNK pathway. Consequently, these data suggest that ColXIII has a role in age-dependent cortical bone deterioration with possible implications for osteoporosis and fracture risk.

中文翻译：

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XIII胶原蛋白的胞外域调节骨血管生成和皮层内重塑。

骨质疏松症是最常见的变性骨骼疾病，发生在骨骼生成和吸收的平衡受到干扰时。骨量减少或其质量改变会导致骨骼明显变弱，从而导致更高的骨折风险。胶原蛋白XIII（ColXIII）是在许多间充质组织中表达的一种保守的跨膜蛋白。在这里，我们显示ColXIII是骨重塑利基的调节剂。在这项研究中，我们发现骨质疏松患者的ColXIII表达明显上调。有鉴于此，我们研究了72周龄以上过表达ColXIII的小鼠（Col13a1oe）的骨稳态，观察到皮质骨过度生长，继而出现严重的骨质流失，以及骨骼血管形成的增加。而且，我们的结果表明，ColXIII衍生的胞外域通过β1-整合素和JNK途径增强血管生成。因此，这些数据表明ColXIII在年龄相关的皮质骨退化中起作用，可能对骨质疏松症和骨折风险具有影响。