Tags

Type your tag names separated by a space and hit enter

Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin-1, and epidermal growth factor in human fibroblasts.
J Cell Physiol. 1987 Aug; 132(2):271-8.JC

Abstract

Tumor necrosis factor (TNF), interleukin-1 (IL-1), and epidermal growth factor (EGF) were mitogenic for human diploid FS-4 fibroblasts. Dexamethasone amplified the growth-stimulating action of all three agents. Amplification of the growth-stimulating action was maximal when dexamethasone was added along with TNF or EGF; no amplification was seen if the addition of dexamethasone was delayed for more than 3 hr. Prolonged simultaneous treatment with TNF and EGF resulted in less growth stimulation than treatment with EGF alone. Dexamethasone abolished this apparent antagonistic interaction between TNF and EGF. Dexamethasone also inhibited the antiviral action of TNF against encephalomyocarditis (EMC) virus in FS-4 cells. TNF and IL-1 increased the steady state level of interferon (IFN)-beta 2 mRNA but failed to induce detectable levels of IFN-beta 1 mRNA in FS-4 cells. Dexamethasone inhibited the increase of IFN-beta 2 mRNA levels by IL-1 or TNF. Inhibition of IFN-beta synthesis is likely to be responsible for the inhibition of the TNF-induced antiviral state by dexamethasone. Since IFNs suppress cell growth, inhibition of endogenous IFN-beta synthesis may also be responsible for the amplification by dexamethasone of the growth-stimulating action of TNF and IL-1. Amplification of the mitogenic action of EGF by dexamethasone appears to be mediated by different mechanism.

Authors

Kohase M
No affiliation info available
Henriksen-Destefano D
No affiliation info available
Sehgal PB
No affiliation info available
Vilcek J
No affiliation info available

MeSH

Cell LineDexamethasoneDrug InteractionsEncephalomyocarditis virusEpidermal Growth FactorFeedbackFibroblastsGlycoproteinsHumansInterferon Type IInterleukin-1MitosisRNA, MessengerTumor Necrosis Factor-alpha

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3040777

Citation

Kohase, M, et al. "Dexamethasone Inhibits Feedback Regulation of the Mitogenic Activity of Tumor Necrosis Factor, Interleukin-1, and Epidermal Growth Factor in Human Fibroblasts." Journal of Cellular Physiology, vol. 132, no. 2, 1987, pp. 271-8.
Kohase M, Henriksen-Destefano D, Sehgal PB, et al. Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin-1, and epidermal growth factor in human fibroblasts. J Cell Physiol. 1987;132(2):271-8.
Kohase, M., Henriksen-Destefano, D., Sehgal, P. B., & Vilcek, J. (1987). Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin-1, and epidermal growth factor in human fibroblasts. Journal of Cellular Physiology, 132(2), 271-8.
Kohase M, et al. Dexamethasone Inhibits Feedback Regulation of the Mitogenic Activity of Tumor Necrosis Factor, Interleukin-1, and Epidermal Growth Factor in Human Fibroblasts. J Cell Physiol. 1987;132(2):271-8. PubMed PMID: 3040777.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin-1, and epidermal growth factor in human fibroblasts. AU - Kohase,M, AU - Henriksen-Destefano,D, AU - Sehgal,P B, AU - Vilcek,J, PY - 1987/8/1/pubmed PY - 1987/8/1/medline PY - 1987/8/1/entrez SP - 271 EP - 8 JF - Journal of cellular physiology JO - J Cell Physiol VL - 132 IS - 2 N2 - Tumor necrosis factor (TNF), interleukin-1 (IL-1), and epidermal growth factor (EGF) were mitogenic for human diploid FS-4 fibroblasts. Dexamethasone amplified the growth-stimulating action of all three agents. Amplification of the growth-stimulating action was maximal when dexamethasone was added along with TNF or EGF; no amplification was seen if the addition of dexamethasone was delayed for more than 3 hr. Prolonged simultaneous treatment with TNF and EGF resulted in less growth stimulation than treatment with EGF alone. Dexamethasone abolished this apparent antagonistic interaction between TNF and EGF. Dexamethasone also inhibited the antiviral action of TNF against encephalomyocarditis (EMC) virus in FS-4 cells. TNF and IL-1 increased the steady state level of interferon (IFN)-beta 2 mRNA but failed to induce detectable levels of IFN-beta 1 mRNA in FS-4 cells. Dexamethasone inhibited the increase of IFN-beta 2 mRNA levels by IL-1 or TNF. Inhibition of IFN-beta synthesis is likely to be responsible for the inhibition of the TNF-induced antiviral state by dexamethasone. Since IFNs suppress cell growth, inhibition of endogenous IFN-beta synthesis may also be responsible for the amplification by dexamethasone of the growth-stimulating action of TNF and IL-1. Amplification of the mitogenic action of EGF by dexamethasone appears to be mediated by different mechanism. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/3040777/Dexamethasone_inhibits_feedback_regulation_of_the_mitogenic_activity_of_tumor_necrosis_factor_interleukin_1_and_epidermal_growth_factor_in_human_fibroblasts_ DB - PRIME DP - Unbound Medicine ER -