漆酶结构域蛋白1通过RIP2介导NOD2泛素化促进骨质疏松模型炎症反应

IF 0.1 4区 生物学 Q4 GENETICS & HEREDITY International Journal of Human Genetics Pub Date : 2022-12-15 DOI:10.31901/24566330.2022/22.04.834
Jun Zhang
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引用次数: 0

摘要

本实验旨在阐明漆酶结构域蛋白1 (LACC1)调控环在骨质疏松症进展中的潜在影响。志愿者的血清样本来自研究人员所在的医院。采用卵巢切除法建立小鼠骨质疏松模型。骨质疏松患者LACC1 mRNA表达水平上调。测定骨质疏松小鼠LACC1蛋白及mRNA表达水平。LACC1在体外模型中促进骨质疏松的炎症反应。LACC1促进小鼠骨质疏松。LACC1蛋白互联核苷酸结合寡聚结构域2 (NOD2)/受体相互作用蛋白2 (RIP2)蛋白减少NOD2泛素化。NOD2/RIP2参与了LACC1在骨质疏松模型中的作用。这些发现表明,LACC1通过抑制NOD2泛素化,诱导NOD2- rip2信号传导,从而促进骨质疏松模型的炎症。抑制LACC1调控环为骨质疏松症的治疗提供了新的靶点。
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Laccase Domain-Containing Protein 1 Promoted Inflammation of Osteoporosis Model via NOD2 Ubiquitination by RIP2
The purpose of this experiment was to elucidate the latent influence of Laccase Domain-Containing Protein 1 (LACC1) regulatory loop in the progression of osteoporosis. Serum samples of volunteers were obtained from the researchers’ hospital. Mice were induced by an osteoporosis model using ovariectomy. LACC1 mRNA expression levels were up-regulated in patients with osteoporosis. LACC1 protein and mRNA expression levels in mice with osteoporosis were measured. LACC1 promoted inflammation of osteoporosis in the in vitro model. LACC1 promoted osteoporosis in the mice model. LACC1 protein interlinked nucleotide-binding oligomerisation domain 2 (NOD2)/ receptor interacting protein 2 (RIP2) protein to reduce ubiquitination of NOD2. NOD2/RIP2 participated in the effects of LACC1 in the model of osteoporosis. These findings suggest that LACC1 promoted inflammation of the osteoporosis model via the induction of NOD2-RIP2 signalling by the inhibition of NOD2 ubiquitination. The inhibition of LACC1 regulatory loop provides new targets for treatment of osteoporosis.
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