Suppr超能文献

骨硬化(op/op)小鼠的先天性破骨细胞缺乏症可通过注射巨噬细胞集落刺激因子治愈。

Congenital osteoclast deficiency in osteopetrotic (op/op) mice is cured by injections of macrophage colony-stimulating factor.

作者信息

Kodama H, Yamasaki A, Nose M, Niida S, Ohgame Y, Abe M, Kumegawa M, Suda T

机构信息

Department of Anatomy, Ohu University School of Dentistry, Koriyama, Japan.

出版信息

J Exp Med. 1991 Jan 1;173(1):269-72. doi: 10.1084/jem.173.1.269.

Abstract

Osteopetrotic (op/op) mice have a severe deficiency of osteoclasts, monocytes, and peritoneal macrophages because of a defect in the production of functional macrophage colony-stimulating factor (M-CSF) resulting from a mutation within the M-CSF gene. In this study, we examined whether daily 5-microgram injections of purified recombinant human M-CSF (rhM-CSF) for 14 d would cure these deficiencies in the mutant mice. Monocytes in the peripheral blood of the op/op mice were significantly increased in number after subcutaneous injections of the factor two or three times a day. In contrast, osteopetrosis in the long bones of op/op mice was completely cured by only one injection of rhM-CSF per day. Bone trabeculae in the diaphyses were removed. Many osteoclasts were detected on the surface of bone trabeculae in the metaphyses. Although development of tooth germs of uninjected op/op mice was impaired, rhM-CSF injection restored the development of molar tooth germs and led to tooth eruption as a consequence of the recovery of bone-resorbing activity. These results demonstrate that M-CSF is one of the factors responsible for the differentiation of osteoclasts and monocyte/macrophages under physiological conditions.

摘要

骨石化(op/op)小鼠由于M-CSF基因内的突变导致功能性巨噬细胞集落刺激因子(M-CSF)产生缺陷,从而严重缺乏破骨细胞、单核细胞和腹腔巨噬细胞。在本研究中,我们检测了每天注射5微克纯化的重组人M-CSF(rhM-CSF),持续14天是否能治愈突变小鼠的这些缺陷。每天皮下注射该因子两到三次后,op/op小鼠外周血中的单核细胞数量显著增加。相比之下,op/op小鼠长骨的骨石化仅通过每天注射一次rhM-CSF就完全治愈了。骨干中的骨小梁被清除。在干骺端的骨小梁表面检测到许多破骨细胞。虽然未注射的op/op小鼠牙胚的发育受损,但rhM-CSF注射恢复了磨牙牙胚的发育,并由于骨吸收活性的恢复导致牙齿萌出。这些结果表明,M-CSF是生理条件下破骨细胞和单核细胞/巨噬细胞分化的相关因子之一。

相似文献

引用本文的文献

5
The osteocyte and its osteoclastogenic potential.成骨细胞及其成骨细胞生成潜能。
Front Endocrinol (Lausanne). 2023 May 24;14:1121727. doi: 10.3389/fendo.2023.1121727. eCollection 2023.
8
The M-CSF receptor in osteoclasts and beyond.破骨细胞中的 M-CSF 受体及其功能。
Exp Mol Med. 2020 Aug;52(8):1239-1254. doi: 10.1038/s12276-020-0484-z. Epub 2020 Aug 17.
9
Vitamin D Inhibition of TRPV5 Expression During Osteoclast Differentiation.破骨细胞分化过程中维生素D对TRPV5表达的抑制作用
Int J Endocrinol Metab. 2019 Oct 14;17(4):e91583. doi: 10.5812/ijem.91583. eCollection 2019 Oct.

本文引用的文献

4
Cellular differences in acid phosphatase isoenzymes in bone and teeth.
Clin Orthop Relat Res. 1971;78:151-67. doi: 10.1097/00003086-197107000-00012.
6
Regulation of new osteoclast formation by a bone cell-derived macromolecular factor.
Biochem Biophys Res Commun. 1989 Mar 31;159(3):1383-90. doi: 10.1016/0006-291x(89)92263-8.
7
Osteoclast formation from cloned pluripotent hemopoietic stem cells.
Bone Miner. 1989 May;6(2):179-89. doi: 10.1016/0169-6009(89)90049-4.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验