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  • Title: Cross talk of tumor necrosis factor-alpha and epidermal growth factor in human microvascular endothelial cells.
    Author: Izumi H, Ono M, Ushiro S, Kohno K, Kung HF, Kuwano M.
    Journal: Exp Cell Res; 1994 Oct; 214(2):654-62. PubMed ID: 7523156.
    Abstract:
    Our previous studies imply that tumor necrosis factor-alpha (TNF-alpha) and epidermal growth factor (EGF) might share a common signal transduction pathway in human omental microvascular endothelial (HOME) cells. Exposure of cultured HOME cells to TNF-alpha for 10 min enhanced EGF receptor phosphorylation at a rate comparable to EGF. Apparent phosphorylation of tyrosine residues was observed in addition to serine/threonine of the EGF receptor by EGF, but only a slightly if any tyrosine phosphorylation by TNF-alpha. In vitro kinase activity of EGF receptor was also enhanced by TNF-alpha as well as by EGF. Furthermore, expression of the c-fos gene was enhanced in response to either EGF or TNF-alpha. Pretreatment of HOME cells with EGF for 12 h almost completely blocked the induction of the c-fos gene by EGF and partially blocked the c-fos induction by TNF-alpha. TNF-alpha-induced c-fos gene expression appeared to be partly due to its transactivation of EGF receptor. EGF and TNF-alpha could enhance c-fos gene expression when protein kinase C was down-regulated by phorbol ester myristate (PMA). Gel retardation assay with the NF-kappa B consensus sequence showed that NF-kappa B binding activity was dramatically activated by TNF-alpha, but not by EGF or PMA. The binding of another transcription factor, AP-1 (Jun/Fos), was enhanced by EGF, TNF-alpha, and PMA, whereas TNF-alpha could still activate AP-1 after longer exposure to EGF. TNF-alpha-induced activation of c-fos gene appears to be mediated through pleiotropic mechanisms and partly through a common signal with EGF, possibly through EGF receptor in microvascular endothelial cells.
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