Cutting edge: Parathyroid hormone facilitates macrophage efferocytosis in bone marrow via proresolving mediators resolvin D1 and resolvin D2.
Cutting edge: Parathyroid hormone facilitates macrophage efferocytosis in bone marrow via proresolving mediators resolvin D1 and resolvin D2.
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DOI：
10.4049/jimmunol.1301945
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发表时间：
2014-07-01
期刊：
影响因子：
--
通讯作者：
Serhan CN
中科院分区：
文献类型：
--
作者：
McCauley LK;Dalli J;Koh AJ;Chiang N;Serhan CN
骨髓巨噬细胞通过尚未明确的机制刺激骨骼伤口修复和成骨细胞骨形成。炎症的专门促消退介质驱动巨噬细胞胞吞作用（凋亡细胞的吞噬作用）和消退，但对于骨髓中的这一过程知之甚少。在本报告中，通过液相色谱质谱法进行的代谢脂组学分析显示，相对于脾脏，骨髓中专门的促溶解介质（SPM）水平更高。内分泌和骨合成代谢剂甲状旁腺激素 (PTH) 增加了 SPM 水平，包括骨髓中的消退素 (Rv)。人类和小鼠原代巨噬细胞在体外吞噬凋亡的成骨细胞，resolvin (Rv) D1 和 RvD2 (10 pM-10 nM) 增强了这一过程。这些发现支持骨髓中特殊脂质介质的独特特征，有助于解决炎症和维持骨骼稳态的反馈系统。
Bone marrow macrophages stimulate skeletal wound repair and osteoblastic bone formation by as yet poorly defined mechanisms. Specialized pro-resolving mediators of inflammation drive macrophage efferocytosis (phagocytosis of apoptotic cells) and resolution but little is known regarding this process in the bone marrow. In the present report, metabololipidomic profiling via liquid chromatographic mass spectrometry revealed higher levels of specialized pro-resolving mediators (SPM) in the bone marrow relative to the spleen. The endocrine and bone anabolic agent parathyroid hormone (PTH) increased SPM levels including resolvins (Rv) in bone marrow. Human and murine primary macrophages efferocytosed apoptotic osteoblasts in vitro, and resolvin (Rv) D1 and RvD2 (10 pM-10 nM) enhanced this process. These findings support a unique profile of specialized lipid mediators in bone marrow that contributes to a feedback system for resolution of inflammation and maintenance of skeletal homeostasis.
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影响因子：
82.9
作者：
通讯作者：
--
影响因子：
4
作者：
Serhan, Charles N.;Chiang, Nan
通讯作者：
Chiang, Nan
影响因子：
5.4
作者：
Schif-Zuck, Sagie;Gross, Nufar;Assi, Simaan;Rostoker, Ran;Serhan, Charles N.;Ariel, Amiram
通讯作者：
Ariel, Amiram
影响因子：
4.8
作者：
Cho, Sun Wook;Pirih, Flavia Q.;McCauley, Laurie K.
通讯作者：
McCauley, Laurie K.
影响因子：
4.8
作者：
Li, Xin;Qin, Ling;Partridge, Nicola C.
通讯作者：
Partridge, Nicola C.