PGE 2 confers survivin-dependent apoptosis resistance in human monocyte-derived dendritic cells Felicita Baratelli, Kostyantyn Krysan, Nathalie Heuzé-Vourc’h, Li Zhu, Brian Escuadro, Sherven Sharma, Karen Reckamp, Mariam Dohadwala and Steven M. Dubinett 1 UCLA Lung Cancer Research Program of the Jonsson Comprehensive Cancer Center and the Division of Pulmonary and Critical Care Medicine, Department of Medicine, Geffen School of Medicine at University of California Los Angeles; and Molecular Gene Medicine Laboratory, Veteran’s Affairs Greater Los Angeles Healthcare System, California 1 Correspondence: Lung Cancer Research Program, Division of Pulmonary and Critical Care Medicine, UCLA Geffen School of Medicine, 37-131 CHS, 10833 Le Conte Ave., Room 37-131 CHS, Los Angeles, CA 90095. E-mail: sdubinett@mednet.ucla.edu Control of apoptosis is fundamental for dendritic cell (DC) homeostasis. Numerous factors maintain DC viability throughout their lifespan, including inhibitor of apoptosis proteins. Among them, survivin is overexpressed in many human malignancies, but its physiological function in normal cells has not been fully delineated. Prostaglandin E 2 (PGE 2 ), also overproduced in several malignancies, has shown to induce proapoptotic and antiapoptotic effects in different cell types, including immune cells. In DC, PGE 2 predominantly affects maturation and modulates immune functions. Here, we show that exposure of monocyte-derived DC to PGE 2 (10 – 5 M) for 72 h significantly increased DC survivin mRNA and protein expression. In contrast, DC, matured with lipopolysaccharide or tumor necrosis factor α, did not reveal survivin induction in response to PGE 2 . Following exposure to apoptotic stimuli, DC treated with PGE 2 exhibited an overall increased viability compared with control DC, and this effect was correlated inversely with caspase-3 activation. Moreover, PGE 2 -treated, survivin-deficient DC demonstrated reduced viability in response to apoptotic stimuli. Further analysis indicated that PGE 2 induced DC survivin expression in an E prostanoid (EP) 2 /EP 4 receptor and phosphatidylinositol-3 kinase-dependent manner. These findings suggest that PGE 2 -dependent regulation of survivin is important in modulating apoptosis resistance in human DC. Key Words: lipid mediators • immune cells • antiapoptotic proteins
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PGE2 confers survivin-dependent apoptosis resistance in human monocyte-derived dendritic cells
Baratelli, Felicita; Krysan, Kostyantyn; Heuzé-Vourch, Nathalie; Zhu, Li; Escuadro, Brian; Sharma, Sherven; Reckamp, Karen; Dohadwala, Mariam; Dubinett, Steven M.
Follow Journal of Leukocyte Biology
, Volume 78 (2): 555
Fed of American Socs for Experimental Biology – Aug 1, 2005
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