Secretion of Transforming Growth Factor-β1 and -β2 by Malignant Glioma Cells

The secretion of transforming growth factor-β (TGF-fl), a growth inhibitory factor with immunosuppressive properties, was investigated in one glioblastoma cell line and seven surgically resected malignant glioma cells. Cultured cells from surgically resected tumors were examined immunohistochemicall...

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Veröffentlicht in:Neurologia medico-chirurgica 1995, Vol.35(7), pp.423-430
Hauptverfasser: SASAKI, Atsushi, NAGANUMA, Hirofumi, SATOH, Eiji, NAGASAKA, Mitsuyasu, ISOE, Shiro, NAKANO, Shin, NUKUI, Hideaki
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Sprache:eng
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Zusammenfassung:The secretion of transforming growth factor-β (TGF-fl), a growth inhibitory factor with immunosuppressive properties, was investigated in one glioblastoma cell line and seven surgically resected malignant glioma cells. Cultured cells from surgically resected tumors were examined immunohistochemically for glial fibrillary acidic protein (GFAP) and S-100 protein. The levels of TGF-/β and TGF-/β2 in culture supernatants from malignant glioma cells were determined by a specific bioassay using antiTGF-/β1 and anti-TGF-/β2 antibodies. Two glioblastoma cell lines were cultured in the presence of TGF-/β1 or TGF-/β2 to assess the effect of TGF-β on the growth of glioblastoma cells. Cultured cells from surgically resected tumors were positive for both GFAP and S-100 protein. Both active and latent forms of TGF-/β1 and TGF-/β2 were detected in the culture supernatants from malignant gliomas, except in one patient with anaplastic astrocytoma which secreted only latent forms of TGF-/β1 and TGF/β2. There was no statistical difference in the levels of TGF-, β1 and TGF-/β2 in glioblastomas and anaplastic astrocytomas. Neither TGF-/β1 nor TGF-/β2 affected the growth of glioblastoma cells. These findings suggest that most malignant glioma cells secrete both TGF-/βl and TGF-/β2, can convert TGF/β from a latent to active form, and may suppress cytokine secretion by activated lymphocytes in vivo as well as in vitro.
ISSN:0470-8105
1349-8029
DOI:10.2176/nmc.35.423