Parathyroid hormone induces bone resorption in human peripheral blood mononuclear cells
Parathyroid hormone induces bone resorption in human peripheral blood mononuclear cells
复制标题
甲状旁腺激素诱导人外周血单核细胞骨吸收
DOI：
10.1046/j.1365-2613.1998.00020.x
复制
发表时间：
1998
影响因子：
3
通讯作者：
Chambers
中科院分区：
文献类型：
--
作者：
Fuller;Chambers
已知破骨细胞源自巨噬细胞集落刺激因子（M - CSF）依赖性前体，与巨噬细胞共享。能够形成破骨细胞的细胞存在于外周血中。我们将人外周血单核细胞（PBMCs）与破骨细胞诱导的UMR 106细胞、人巨噬细胞集落刺激因子（hM - CSF）和甲状旁腺激素（PTH）或125 (OH) 2维生素D3一起培养在失活的皮质骨切片上，对这一群体进行了表征。我们发现pbmc能够大量的骨吸收，达到与造血组织相当的水平。在极低密度下镀细胞并筛选是否存在挖掘，发现镀细胞数量与形成的挖掘数量之间存在线性关系（r = 0.994）。极限稀释分析表明，每300-600个镀膜细胞中有1个（占PBMC群体的0.15-0.3%）具有骨吸收能力。在快速粘附的部分中发现了前体，并且通常产生很少数量的挖掘，这表明它是一种相对成熟的细胞类型。pbmc与UMR 106细胞共培养，如果没有PTH/1,25(OH)2维生素D3，即使有M - CSF，也不会产生破骨细胞，这表明基质细胞诱导破骨细胞不是由于UMR 106细胞中M - CSF的激素诱导，而是PTH诱导了UMR 106细胞中破骨细胞而不是巨噬细胞形成所必需的其他活性。如果在培养期的前几天忽略PTH，破骨细胞不会形成。因此，破骨细胞似乎不是由巨噬细胞分化的细胞形成的，而是由相对成熟的双电位或破骨细胞前体的离散亚群形成的，在缺乏破骨细胞诱导刺激的情况下，这些前体不可逆转地丧失在破骨细胞谱系中。
Osteoclasts are known to derive from a macrophage colony‐stimulating factor (M‐CSF)‐dependent precursor shared with macrophages. Cells capable of forming osteoclasts are present in peripheral blood. We characterized this population by incubating human peripheral blood mononuclear cells (PBMCs) with osteoclast‐inductive UMR 106 cells, human macrophage colony stimulating factor (hM‐CSF) and parathyroid hormone (PTH) or 1,25(OH)2vitamin D3 on slices of devitalised cortical bone. We found that PBMCs were capable of substantial bone resorption, to levels comparable to those of haemopoietic tissue. Cells plated at very low densities and screened for the presence or absence of excavations revealed a linear relationship (r = 0.994) between the number of cells plated and the number of excavations formed. The limiting dilution analysis suggested that 1 in every 300–600 plated cells (0.15–0.3% of the PBMC population) had the capacity to resorb bone. The precursor was found in the rapidly adherent fraction, and typically generated very small numbers of excavations, suggesting that it was a relatively mature cell type. Co‐cultures of PBMCs with UMR 106 cells would not generate osteoclasts without PTH/1,25(OH)2vitamin D3, even with M‐CSF, indicating that osteoclast‐induction by stromal cells is not attributable to hormonal induction of M‐CSF in UMR 106 cells, but that PTH induces some other activity, necessary for osteoclast but not macrophage formation, in UMR 106 cells. Osteoclasts did not form if PTH was omitted in the first few days of the culture period. Thus, osteoclasts appear to form not from cells committed to macrophage differentiation, but from a discrete subpopulation of relatively mature bipotential or osteoclast‐committed precursors which, in the absence of an osteoclast‐inductive stimulus, become irreversibly lost to the osteoclast lineage.
破骨细胞的起源：骨骼外来源的证据、临床意义和研究挑战。
DOI：
10.1111/j.1600-0714.1983.tb00337.x
发表时间：
1983
期刊：
Journal of oral pathology
影响因子：
--
作者：
MarksJr,SC
通讯作者：
MarksJr,SC
人类集落刺激因子 1 受体中酪氨酸 809 处的点突变会损害有丝分裂，但不会消除酪氨酸激酶活性、与磷脂酰肌醇 3-激酶的关联或 c-fos 和 junB 基因的诱导。
DOI：
10.1073/pnas.87.17.6738
发表时间：
1990
影响因子：
11.1
作者：
Roussel,MF;Shurtleff,SA;Downing,JR;Sherr,CJ
通讯作者：
Sherr,CJ