Chambers T J, Magnus C J
J Pathol. 1982 Jan;136(1):27-39. doi: 10.1002/path.1711360104.
Osteoclasts were incubated on a glass or plastic substrate and the effect of calcitonin (CT) on their behaviour was observed. Before exposure to CT the osteoclasts were actively motile, the cytoplasm advancing behind broad pseudopodial (lamellipodial) processes which showed intense ruffling activity. CT caused cessation of lamellipodial activity within minutes, followed by gradual fragmentation and retraction of lamellipodia. Complete osteoclast quiescence was regularly induced by concentrations of CT above 50 pg/ml, and lesser degrees of quiescence were induced at concentrations down to 10 pg/ml. This quiescent state was reversed on removing CT from the medium, and was abrogated by prior treatment of osteoclasts with trypsin. The quiescent state did not reduce the longevity of the cells in culture, nor did it affect their resistance to removal from glass by trypsin. CT showed no influence on the pseudopodial activity of osteoclasts, peritoneal macrophages or inflammatory giant cells. Osteoclast quiescence seems to be a reversible state induced by the interaction of CT with a trypsin-sensitive CT receptor, present on osteoclasts. The range of concentrations which induce partial osteoclast quiescence are within the physiological range of serum concentrations in man, and this suggests that CT plays a physiological role in the regulation of osteoclasts may help to identify the precursor cell of the osteoclast and may assist investigations into the mechanism of control of osteoclasis.
将破骨细胞接种在玻璃或塑料基质上,观察降钙素(CT)对其行为的影响。在接触CT之前,破骨细胞活动活跃,细胞质在宽阔的伪足(片状伪足)突起后推进,伪足表现出强烈的波动活动。CT在数分钟内导致片状伪足活动停止,随后片状伪足逐渐碎片化并回缩。浓度高于50 pg/ml的CT通常可诱导破骨细胞完全静止,浓度低至10 pg/ml时也可诱导一定程度的静止。从培养基中去除CT后,这种静止状态可逆转,并且在用胰蛋白酶预先处理破骨细胞后,静止状态被消除。静止状态并未降低培养细胞的寿命,也不影响它们对胰蛋白酶从玻璃上去除的抵抗力。CT对破骨细胞、腹腔巨噬细胞或炎性巨细胞的伪足活动没有影响。破骨细胞静止似乎是一种由CT与破骨细胞上存在的对胰蛋白酶敏感的CT受体相互作用诱导的可逆状态。诱导破骨细胞部分静止的浓度范围在人类血清浓度的生理范围内,这表明CT在破骨细胞调节中起生理作用,可能有助于识别破骨细胞的前体细胞,并可能有助于研究破骨作用的控制机制。