Interferon-gamma modulates messenger RNA levels of c-sis (PDGF-B chain), PDGF-A chain, and IL-1 beta genes in human vascular endothelial cells

• Published in: The American journal of pathology Vol. 134; no. 1; pp. 35 - 43
• Main Authors: Suzuki, H, Shibano, K, Okane, M, Kono, I, Matsui, Y, Yamane, K, Kashiwagi, H
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01-01-1989; American Society for Investigative Pathology
• Subjects: Biological and medical sciences; Cells, Cultured; Dose-Response Relationship, Drug; Endothelium, Vascular - cytology; Endothelium, Vascular - metabolism; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation - drug effects; Genes; Humans; Interferon-gamma - pharmacology; Interferon-gamma - physiology; Interleukin-1 - genetics; Interleukin-1 - pharmacology; Molecular and cellular biology; Molecular genetics; Platelet-Derived Growth Factor - genetics; RNA, Messenger - metabolism; Stereoisomerism; Tumor Necrosis Factor-alpha - pharmacology; Human; Endothelial cell; Regulation(control); Messenger RNA; C-Onc gene; Blood vessel; Interleukin 1β; Gene expression; Platelet derived growth factor; Gamma interferon
• ISSN: 0002-9440; 1525-2191

The authors have investigated the effects of cytokines and lipopolysaccharide (LPS) on mRNA levels of c-sis (platelet-derived growth factor (PDGF)-B chain), PDGF-A chain, and interleukin 1 beta (IL-1 beta) genes in human vascular endothelial cells (EC). IL-1, tumor necrosis factor (TNF), and LPS not only enhanced the accumulation of c-sis mRNA, but also induced IL-1 beta gene expression. Interferon-gamma (IFN-gamma), in contrast, suppressed the accumulation of c-sis mRNA profoundly and PDGF-A chain mRNA to a lesser extent. The cytokine, in addition, suppressed the release of PDGF-like proteins by EC, while maintaining the growth of EC. IFN-gamma, however, augmented the levels of IL-1 beta mRNA in cultured EC in association with LPS or IL-1, suggesting that the suppression of c-sis expression was not mediated through modulation of IL-1 gene expression by IFN-gamma. These results raise the possibility that IFN-gamma may play a novel regulatory role in the pathogenesis of vascular diseases such as atherosclerosis and vasculitis.