ABILITY OF INSULIN AND DSRNA TO INDUCE INTERFERON SYSTEM AND HSP-70 IN FIBROBLAST AND EPITHELIAL-CELLS IN RELATION TO THEIR EFFECTS ON CELL-GROWTH

Citation
Mk. Chelbialix et Ce. Sripati, ABILITY OF INSULIN AND DSRNA TO INDUCE INTERFERON SYSTEM AND HSP-70 IN FIBROBLAST AND EPITHELIAL-CELLS IN RELATION TO THEIR EFFECTS ON CELL-GROWTH, Experimental cell research, 213(2), 1994, pp. 383-390
Citations number
56
Categorie Soggetti
Oncology,"Cytology & Histology
Journal title
ISSN journal
00144827
Volume
213
Issue
2
Year of publication
1994
Pages
383 - 390
Database
ISI
SICI code
0014-4827(1994)213:2<383:AOIADT>2.0.ZU;2-T
Abstract
We have examined the ability of insulin and dsRNA, a well-known interf eron inducer, in relation to their effects on cell growth, to induce t he expression of hsp 70 and the synthesis of interferon in epithelial HT-29 and fibroblast Madin-Darby bovine kidney (MDBK) cells. Insulin w as mitogenic in both MDBK and HT-29 cells; MDBR cells nevertheless req uired much higher concentrations. DsRNA stimulated the growth of MDBK but inhibited that of HT-29 cells. Both substances induced a transient synthesis of hsp 70 in HT-29 and MDBK cells with similar kinetics. Ho wever, whereas both insulin and dsRNA efficiently induced 2'5' oligoad enylate synthetase and an antiviral state through interferon synthesis in HT-29 cells, only dsRNA caused these effects in MDBK cells. Thus, insulin cannot, unlike dsRNA, elicit an antiviral state in all cell sy stems, although, like dsRNA, it can induce hsp 70, thereby suggesting the cell specificity of insulin action. These results reveal that the mitogenic and IFN-inducing effects of insulin and dsRNA are dependent on the cell type and unrelated to hsp 70 expression. (C) 1994 Acndemic Press, Inc.