Transforming growth factor (TGF) beta l enhanced in vitro [H-3]thymidine in
corporation into C6 cells and reduced that of astrocytes in the presence of
a high serum concentration. It concomitantly raised the gap junction inter
cellular communication (GJIC) in normal astrocytes but reduced the coupling
of Cb cells, and respectively increased or decreased the proportion of P-2
-phosphorylated connexin (Cx) 43 isoform in these cells. Finally, octanol,
which inhibited GJIC in both cell types, increased the thymidine incorporat
ion in C6 cells, but neither altered the proliferation of astrocytes nor th
eir response to TGF beta l. These data indicate that an inhibition of gap j
unction intercellular communication, due to an altered phosphorylation of c
onnexin 43, may contribute to the proliferative response of C6 glioblastoma
cells to TGF beta l. NeuroReport 11:2837-2841 (C) 2000 Lippincott Williams
& Wilkins.