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甲状旁腺激素相关蛋白(PTHrP)在牙周膜细胞中诱导Notch信号传导。

PTHrP induces Notch signaling in periodontal ligament cells.

作者信息

Nakao A, Kajiya H, Fukushima H, Fukushima A, Anan H, Ozeki S, Okabe K

机构信息

Department of Physiological Science and Molecular Biology, Fukuoka Dental College, 2-15-1 Tamura, Sawara-ku, Fukuoka 814-0193, Japan.

出版信息

J Dent Res. 2009 Jun;88(6):551-6. doi: 10.1177/0022034509337899.

Abstract

Periodontal ligament (PDL) cells are known to play important roles in tooth eruption and alveolar bone metabolism. We previously reported that PTHrP increases RANKL expression in human PDL cells, suggesting that it promotes odontoclastic root resorption during tooth eruption. While it is known that Notch-related genes play a key role during bone development, the role of the Notch signaling pathway in PDL cells during tooth and bone resorption is less clear. We hypothesized that PTHrP induces a Notch ligand in PDL cells and thereby regulates osteo- and odontoclastogenesis. We found that PTHrP increased Notch1 ligand Jagged1 expression in human PDL cells in a dose- and time-dependent manner. PTHrP-induced Jagged1 up-regulation was mediated by PKA activation, but not by PKC. Jagged1 also promoted RANKL-induced osteoclastogenesis. These results demonstrate that PTHrP induces Jagged1 expression in PDL cells, leading to osteo- and odontoclastogenesis, and thus likely promoting tooth and alveolar bone resorption.

摘要

已知牙周韧带(PDL)细胞在牙齿萌出和牙槽骨代谢中发挥重要作用。我们之前报道过,甲状旁腺激素相关蛋白(PTHrP)会增加人牙周韧带细胞中核因子κB受体活化因子配体(RANKL)的表达,这表明它在牙齿萌出过程中促进破牙细胞性牙根吸收。虽然已知Notch相关基因在骨骼发育过程中起关键作用,但Notch信号通路在牙齿和骨骼吸收过程中在牙周韧带细胞中的作用尚不清楚。我们推测PTHrP在牙周韧带细胞中诱导一种Notch配体,从而调节成骨细胞和破骨细胞生成。我们发现PTHrP以剂量和时间依赖性方式增加人牙周韧带细胞中Notch1配体锯齿状蛋白1(Jagged1)的表达。PTHrP诱导的Jagged1上调是由蛋白激酶A(PKA)激活介导的,而非蛋白激酶C(PKC)。Jagged1也促进RANKL诱导的破骨细胞生成。这些结果表明,PTHrP在牙周韧带细胞中诱导Jagged1表达,导致成骨细胞和破牙细胞生成,从而可能促进牙齿和牙槽骨吸收。

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