Regulation of osteoclast function by AMPK activity

AMPK是一种代谢主开关，调节细胞对营养环境变化的适应。它的活性是由细胞内AMP/ATP比率的增加来刺激的，以应对运动、缺氧和缺糖等应激反应。为了测试调节AMPK活性是否会影响破骨细胞的功能，我们使用了含有显性阴性形式(a1dN，a2dN)或成分活性形式(a1CA，a2CA)的AMPK催化亚基(a1和a2)的腺病毒载体。AMPK的直接靶点Ser-79的乙酰辅酶A羧基酶的磷酸化水平受腺病毒介导的AMPK突变体表达的调节。AMPK活性的调节不影响破骨细胞存活或骨吸收，表明AMPK不参与ATP耗竭诱导的骨吸收。

AMPK is a metabolic master switch that mediates the adaptation of the cell to variations in the nutritional environment. Its activity is stimulated by increases in the intracellular AMP/ATP ratio in response to stresses such as exercise, hypoxia, and glucose deprivation. To test whether modulating AMPK activity would affect osteoclast function, we used adenovirus vectors containing dominant negative (a1DN , a2DN) or constitutively active (a1CA , a2CA) forms of AMPK catalytic subunits (a1 and a2). The phosphorylation level of acetyl-CoA carboxylase at Ser-79, a direct target of AMPK, was modulated by adenovirus-mediated expression of the AMPK mutants. Modulation of AMPK activity did not affect osteoclast survival or bone resorption, indicating that AMPK is not involved in ATP depletion-induced bone resorption.