Growth regulation of astrocytes and C6 cells by TGFβI
- 1 September 2000
- journal article
- Published by Wolters Kluwer Health in NeuroReport
- Vol. 11 (13) , 2837-2841
- https://doi.org/10.1097/00001756-200009110-00003
Abstract
Transforming growth factor (TGF) beta1 enhanced in vitro [3H]thymidine incorporation into C6 cells and reduced that of astrocytes in the presence of a high serum concentration. It concomitantly raised the gap junction intercellular communication (GJIC) in normal astrocytes but reduced the coupling of C6 cells, and respectively increased or decreased the proportion of P2-phosphorylated connexin (Cx) 43 isoform in these cells. Finally, octanol, which inhibited GJIC in both cell types, increased the thymidine incorporation in C6 cells, but neither altered the proliferation of astrocytes nor their response to TGFbeta1. These data indicate that an inhibition of gap junction intercellular communication, due to an altered phosphorylation of connexin 43, may contribute to the proliferative response of C6 glioblastoma cells to TGFbeta1.Keywords
This publication has 7 references indexed in Scilit:
- Progression as exemplified by human astrocytic tumorsSeminars in Cancer Biology, 1999
- CONNEXINS, CONNEXONS, AND INTERCELLULAR COMMUNICATIONAnnual Review of Biochemistry, 1996
- Transforming growth factor‐βs inhibit mitogen‐stimulated proliferation of astrocytesGlia, 1993
- The Hormone-Induced Regulation of Contact-Dependent Cell-Cell Communication by Phosphorylation*Endocrine Reviews, 1990
- The actions of retinoids on cellular growth correlate with their actions on gap junctional communication.The Journal of cell biology, 1989
- Immunohistochemical demonstration of serum proteins in human cerebral gliomasActa Neuropathologica, 1987
- A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye bindingAnalytical Biochemistry, 1976