Preincubation with interleukin-2 (IL-2), a T cell-derived cytokine, enhanced the increase in intracellular Ca2+ ([Ca2+ ](i)) induced by angiotensin II (AII) in vascular smooth muscle cells (VSMC). IL-2 itself did not affect the basal [Ca2+](i) level or the maximal response of [Ca2+](i) increase induced by AII. Furthermore, IL-2-induced enhancement was not observed in the absence of extracellular Ca2+ suggesting that IL-2 enhances Ca2+ influx induced by AII. IL-2 also enhanced the stimulation of DNA synthesis induced by AII, although IL-2 alone did not stimulate DNA synthesis. Genistein, an inhibitor of protein tyrosine kinases, significantly inhibited IL-2-induced enhancement of both Ca2+ influx and DNA synthesis induced by AII. A neutralizing antibody against heparin-binding epidermal growth factor-like growth factor (HB-EGF) partially inhibited IL-2-induced enhancement of DNA synthesis induced by AII. These findings suggest that autocrine HB-EGF is partially involved in the mechanism of IL-2-induced enhancement of DNA synthesis. On the other hand IL-2 stimulated both glycosaminoglycan (GAG) and prostacyclin syntheses and enhanced the stimulation of both GAG and prostacyclin syntheses induced by AII. Therefore, IL-2 may play important roles in the pathogenesis of atherosclerosis and vascular disease by modulating the responsiveness to AII in VSMC.
Pharmacological control of the mevalonate pathway in the regulation of arterial myocyte proliferation / A. Corsini, L. Arnaboldi,P. McGeady, M.H. Gelb, P. Quarato, C. Tagliabue, N. Ferri, R. Paoletti, R. Fumagalli. - In: ATHEROSCLEROSIS. - ISSN 0021-9150. - 133:2(1997), pp. 23-23. ((Intervento presentato al 68. convegno Meeting of the European Atherosclerosis Society (EAS): Molecular Cell Biology and Atherogenesi tenutosi a Brugge (Belgio) nel 1997 [10.1016/S0021-9150(97)00107-X].
Pharmacological control of the mevalonate pathway in the regulation of arterial myocyte proliferation
A. CorsiniPrimo
;L. ArnaboldiSecondo
;N. Ferri;R. PaolettiPenultimo
;
1997
Abstract
Preincubation with interleukin-2 (IL-2), a T cell-derived cytokine, enhanced the increase in intracellular Ca2+ ([Ca2+ ](i)) induced by angiotensin II (AII) in vascular smooth muscle cells (VSMC). IL-2 itself did not affect the basal [Ca2+](i) level or the maximal response of [Ca2+](i) increase induced by AII. Furthermore, IL-2-induced enhancement was not observed in the absence of extracellular Ca2+ suggesting that IL-2 enhances Ca2+ influx induced by AII. IL-2 also enhanced the stimulation of DNA synthesis induced by AII, although IL-2 alone did not stimulate DNA synthesis. Genistein, an inhibitor of protein tyrosine kinases, significantly inhibited IL-2-induced enhancement of both Ca2+ influx and DNA synthesis induced by AII. A neutralizing antibody against heparin-binding epidermal growth factor-like growth factor (HB-EGF) partially inhibited IL-2-induced enhancement of DNA synthesis induced by AII. These findings suggest that autocrine HB-EGF is partially involved in the mechanism of IL-2-induced enhancement of DNA synthesis. On the other hand IL-2 stimulated both glycosaminoglycan (GAG) and prostacyclin syntheses and enhanced the stimulation of both GAG and prostacyclin syntheses induced by AII. Therefore, IL-2 may play important roles in the pathogenesis of atherosclerosis and vascular disease by modulating the responsiveness to AII in VSMC.Pubblicazioni consigliate
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