Hyperglycemia Induces Osteoclastogenesis and Bone Destruction Through the Activation of Ca2+/Calmodulin-Dependent Protein Kinase II

被引:18
作者
Shen, Yanxin [1 ,2 ,3 ]
Guo, Shujuan [1 ,2 ,3 ,4 ]
Chen, Guoqing [1 ,2 ,3 ]
Ding, Yi [1 ,2 ,4 ]
Wu, Yafei [1 ,2 ,4 ]
Tian, Weidong [1 ,2 ,3 ,5 ]
机构
[1] Sichuan Univ, West China Hosp Stomatol, State Key Lab Oral Dis, Chengdu 610041, Peoples R China
[2] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Chengdu 610041, Peoples R China
[3] Sichuan Univ, West China Hosp Stomatol, Natl Engn Lab Oral Regenerat Med, Chengdu 610041, Peoples R China
[4] Sichuan Univ, West China Hosp Stomatol, Dept Periodont, Chengdu 610041, Peoples R China
[5] Sichuan Univ, West China Hosp Stomatol, Dept Oral & Maxillofacial Surg, Chengdu 610041, Peoples R China
基金
中国国家自然科学基金;
关键词
Hyperglycemia; Type 1 diabetes mellitus; Osteoclast; Ca2+; calmodulin-dependent protein kinase II; Bone resorption; DIABETES-MELLITUS; DEPENDENT KINASE; GLYCEMIC CONTROL; CAMKII; EXPRESSION; DIFFERENTIATION; RATS; MICROARCHITECTURE; DYSFUNCTION; MECHANISMS;
D O I
10.1007/s00223-018-0499-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hyperglycemia induces osteoclastogenesis and bone resorption through complicated, undefined mechanisms. Ca2+/calmodulin-dependent protein kinase II (CaMKII) promotes osteoclastogenesis, and could be activated by hyperglycemia. Here, we investigated whether CaMKII is involved in hyperglycemia-induced osteoclastogenesis and subsequent bone resorption. Osteoclast formation, bone resorption, CaMKII expression and phosphorylation were measured under high glucose in vitro and in streptozotocin-induced hyperglycemia rats with or without CaMKII inhibitor KN93. The results showed that 25mmol/L high glucose in vitro promoted cathepsin K and tartrate-resistant acid phosphatase expression (p<0.05) and osteoclast formation (p<0.01) associated with enhancing isoform expression (p<0.05) and CaMKII phosphorylation (p<0.001). Hyperglycemia promoted the formation of osteoclasts and resorption of trabecular and alveolar bone, and inhibited sizes of femur and mandible associated with enhanced CaMKII phosphorylation (p<0.001) in rats. All these changes could be alleviated by KN93. These findings imply that CaMKII participates not only in hyperglycemia-induced osteoclastogenesis and subsequent bone resorption, but also in the hyperglycemia-induced developmental inhibition of bone.
引用
收藏
页码:390 / 401
页数:12
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