Presence of leukaemia inhibitory factor (LIF) and LIF-receptor chain (gp190) in osteoclast-like cells cultured from human giant cell tumour of bone. Ultrastructural …

F Gouin, S Couillaud, M Cottrel, A Godard, N Passuti… - Cytokine, 1999 - Elsevier
F Gouin, S Couillaud, M Cottrel, A Godard, N Passuti, D Heymann
Cytokine, 1999Elsevier
The behaviour of multinucleated giant cells (MNC) obtained from a giant cell tumour of the
tibia and cultured on glass coverslips or on devitalized dentin slices was investigated using
light and electron microscopy. Cells were studied in the presence or absence of LIF a
cytokine known to be involved in bone turnover and to act as a growth factor in some solid
tumours. The direct effect of LIF on MNC was examined by a post-embedding colloidal gold
immunocytochemistry process using human anti-LIF and anti-LIF-receptor (chain gp190) …
The behaviour of multinucleated giant cells (MNC) obtained from a giant cell tumour of the tibia and cultured on glass coverslips or on devitalized dentin slices was investigated using light and electron microscopy. Cells were studied in the presence or absence of LIF a cytokine known to be involved in bone turnover and to act as a growth factor in some solid tumours. The direct effect of LIF on MNC was examined by a post-embedding colloidal gold immunocytochemistry process using human anti-LIF and anti-LIF-receptor (chain gp190) antibodies. After 7 days of culture, the MNC obtained displayed osteoclast immunocytochemical features. Moreover, these MNC were able to resorb large amounts of dentin and presented typical features of active osteoclasts. Immunolocalization of LIF and LIF-receptor revealed the presence of this cytokine and its receptor within the cytoplasm and nucleus of active resorbing MNC. LIF upmodulated MNC number and nucleation but decreased their ability to resorb dentin. The present study suggests that MNC obtained from human GCT, currently considered as osteoclast-like cells, are targets for LIF and may be a source of LIF production in this pathological condition.
Elsevier