丝裂原活化蛋白激酶磷酸酶-1可预防炎症性骨质流失。
MAP kinase phosphatase-1 protects against inflammatory bone loss.
作者信息
Sartori R, Li F, Kirkwood K L
机构信息
Department of Periodontics, School of Dentistry at Araraquara, São Paulo State University, Araraquara, São Paulo, Brazil.
出版信息
J Dent Res. 2009 Dec;88(12):1125-30. doi: 10.1177/0022034509349306. Epub 2009 Oct 28.
Abstract
The mitogen-activated protein (MAP) kinase phosphatase (MKP) family plays an important function in regulating the pro-inflammatory cytokines by deactivating MAP kinases. MKP-1 is essential for the dephosphorylation of p38 MAP kinase that regulates expression of IL-6, TNF-alpha, and IL-1 beta. We hypothesized that MKP-1 regulates inflammatory bone loss in experimental periodontitis. Wild-type and Mkp-1(-/-) mice received A. actinomycetemcomitans LPS injection in the palatal region or PBS control 3 times/wk for 30 days. Mice were killed, and maxillae were assessed by microcomputed tomography, histological analysis, and TRAP staining for measurement of bone loss, extent of inflammation, and degree of osteoclastogenesis. Results indicated that, in LPS-injected Mkp-1(-/-) mice, significantly greater bone loss occurred with more inflammatory infiltrate and a significant increase in osteoclastogenesis compared with Mkp-1(-/-) control sites or either wild-type group. Analysis of these data indicates that MKP-1 plays a key role in the regulation of inflammatory bone loss.
摘要
丝裂原活化蛋白（MAP）激酶磷酸酶（MKP）家族通过使MAP激酶失活，在调节促炎细胞因子方面发挥重要作用。MKP-1对于调节IL-6、TNF-α和IL-1β表达的p38 MAP激酶的去磷酸化至关重要。我们推测MKP-1在实验性牙周炎中调节炎症性骨丢失。野生型和Mkp-1(-/-)小鼠每周3次在腭部区域注射伴放线放线杆菌脂多糖或PBS对照，持续30天。处死小鼠，通过微型计算机断层扫描、组织学分析和抗酒石酸酸性磷酸酶（TRAP）染色评估上颌骨，以测量骨丢失、炎症程度和破骨细胞生成程度。结果表明，与Mkp-1(-/-)对照部位或野生型组相比，在注射脂多糖的Mkp-1(-/-)小鼠中，骨丢失明显更多，炎症浸润更严重，破骨细胞生成显著增加。对这些数据的分析表明，MKP-1在炎症性骨丢失的调节中起关键作用。
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