17beta-estradiol prevents programmed cell death in cardiac myocytes.

in Biochemical and biophysical research communications (2000), 268(1), 192-200

The cardioprotective effects of estrogens are clearly established. However, the underlying mechanisms are poorly understood. Because programmed cell death (apoptosis) probably contributes to the loss of ... [more ▼]

The cardioprotective effects of estrogens are clearly established. However, the underlying mechanisms are poorly understood. Because programmed cell death (apoptosis) probably contributes to the loss of cardiac myocytes in heart failure and because estrogens prevent apoptosis in breast cancer cells, we investigated whether the loss of cardiac myocytes by programmed cell death could be prevented by physiological doses of 17beta-estradiol. Apoptosis of cultured cardiac myocytes was induced by staurosporine. 17beta-estradiol (10 nM) had an antiapoptotic effect as determined by morphological analysis, vital staining using the Hoechst dye 33342 and terminal transferase dUTP nick-end labeling (TUNEL). As a potential mechanism for the antiapoptotic effect of 17beta-estradiol we found a reduced activity of the ICE-like protease caspase-3 in hormone-treated myocytes. Furthermore, inhibition of apoptosis by estradiol was associated with a reduced activity of NF-kappaB transcription factors, particularly p65/RelA and p50. To our knowledge, these data provide the first indication that 17beta-estradiol in physiological concentrations inhibits apoptosis in cardiac myocytes. The antiapoptotic effect of estrogens might contribute to the known cardioprotective effect of estrogens and provides a starting point for the development of future treatment options. [less ▲]

Das 18. Jahrhundert: eine Beschleunigung

in Hausberger, Bernd; Lehners, Jean-Paul (Eds.) Die Welt im 18. Jahrhundert. (2011)

1839

in Kmec, Sonja; Margue, Michel; Péporté, Pit (Eds.) et al Lieux de mémoire au Luxembourg. Usages du passé et construction nationale / Erinnerungsorte in Luxemburg. Umgang mit der Vergangenheit und Konstruktion der Nation (2007)

1848 - Die erste Revolution des industriellen Zeitalters. Zum Geburtsakt der Luxemburger Arbeiterbewegung

Article for general public (1998)

1867, Napoléon III, Bismarck et un record

Article for general public (2017)

Das 19. Jahrhundert als Mediengesellschaft

in MEDIENwissenschaft: Rezensionen, Reviews (2010), (02), 195-197

1916 - eine Zeit der sozialen Kämpfe beginnt in Luxemburg. Die Gründung des Berg- und Hüttenarbeiterverbandes sowie des Metallarbeiterverbandes

Article for general public (1991)

1919: L'autre référendum

Article for general public (2015)

Weekly column on contemporary history ("L'histoire du temps présent") in Luxembourg newspaper Tageblatt, here on the referendum of 1919 about monarchy or republic for Luxembourg

1933-1939. Die Musikseiten des Tageblatt

Article for general public (2013)

1alpha,25-Dihydroxyvitamin D3 is a potent suppressor of interferon gamma-mediated macrophage activation.

in Blood (2005), 106(13), 4351-8

1alpha,25-Dihydroxyvitamin D3 (1alpha,25(OH)2D3), the activated vitamin D3 hormone, is a key regulator of calcium homeostasis and thereby indispensable for bone metabolism. In addition, 1alpha,25(OH)2D3 ... [more ▼]

1alpha,25-Dihydroxyvitamin D3 (1alpha,25(OH)2D3), the activated vitamin D3 hormone, is a key regulator of calcium homeostasis and thereby indispensable for bone metabolism. In addition, 1alpha,25(OH)2D3 is known to mediate predominantly immunosuppressive responses in vitro and in vivo. It has been demonstrated that macrophages can produce 1alpha,25(OH)2D3 on activation with interferon gamma (IFN-gamma), although little is understood about the biologic significance of this response. We show here that 1alpha,25(OH)2D3 can selectively suppress key effector functions of IFN-gamma-activated macrophages. Among these are the suppression of listericidal activity, the inhibition of phagocyte oxidase-mediated oxidative burst, and the suppression of important IFN-gamma-induced genes, including Ccl5, Cxcl10, Cxcl9, Irf2, Fcgr1, Fcgr3, and Tlr2. The deactivation of IFN-gamma-stimulated macrophages is dependent on a functional vitamin D receptor and 1alpha,25(OH)2D3 acts specifically on IFN-gamma-activated macrophages, whereas the steroid has no effects on resting macrophages. Therefore, the 1alpha,25(OH)2D3-mediated suppression of macrophage functions is distinct from previously described macrophage deactivation mechanisms. In conclusion, our data indicate that the production of 1alpha,25(OH)2D3 by IFN-gamma-stimulated macrophages might be an important negative feedback mechanism to control innate and inflammatory responses of activated macrophages. [less ▲]