Abstract
We previously found that TGF-β 1 inhibits PDGF mitogenicity in MG-63 cells and the inhibition is correlated with a suppression of the PDGF-induced receptor autophosphorylation. In this study, we analyze if all the PDGF receptor signaling pathways are similarly affected by the TGF-β1 pretreatment. We show that TGF-β1 suppresses PDGF-stimulated tyrosine phosphorylation of PLC-γ1, and the phosphorylation of Erk. In contrast, the tyrosine phosphorylation of P13-kinase is not affected. Thus, TGF-β1 selectively suppresses two out of three PDGF receptor signaling pathways despit of its prominent inhibition of the PDGF-induced receptor autophosphorylation. The results also indicate that activation of the P13-kinase pathway alone by PDGF is not sufficient in supporting the optimum growth of MG-63 cells under the culture conditions employed.
| Original language | English |
|---|---|
| Pages (from-to) | 685-693 |
| Number of pages | 9 |
| Journal | Life Sciences |
| Volume | 61 |
| Issue number | 7 |
| DOIs | |
| State | Published - 11 07 1997 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- MG-63 cells
- PDGF receptor signalling pathways
- Platelet derived growth factor
- TGF-β1
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