Modulation of thymocyte apoptosis by isoproterenol and prostaglandin E2

• Published in: Cellular immunology Vol. 134; no. 1; pp. 235 - 240
• Main Authors: SUZUKI, K, TADAKUMA, T, KIZAKI, H
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier 15.04.1991
• Subjects: Animals; Biological and medical sciences; Cell physiology; Cell Survival - drug effects; Cyclic AMP - physiology; Dinoprostone - pharmacology; DNA Damage; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Isoproterenol - pharmacology; L-Lactate Dehydrogenase - metabolism; Lymphocytes - cytology; Male; Mice; Mice, Inbred BALB C; Molecular and cellular biology; Protein Kinase C - physiology; Responses to growth factors, tumor promotors, other factors; Tetradecanoylphorbol Acetate - pharmacology; Thymus Gland - cytology; Thymocyte; Arachidonic acid derivatives; Rodentia; Cyclic AMP; Prostaglandin E2; Fragmentation; Signal transduction; Vertebrata; Mammalia; Mouse; Cell death; DNA; Modulation; Mechanism of action; Lymphocyte
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1016/0008-8749(91)90346-d

Isoproterenol and prostaglandin E2 increased cAMP levels in mouse thymocytes transiently, but failed to induce significant internucleosomal DNA fragmentation in thymocytes with a 24-hr incubation. However, these substances showed synergistic interaction with forskolin in the accumulation of cAMP and DNA fragmentation. The addition of 12-O-tetradecanoyl 13-acetate, an activator of protein kinase C, with isoproterenol or particularly with prostaglandin E2 enhanced DNA fragmentation. These results indicate that an increase in cAMP mediated by isoproterenol or prostaglandin receptor is involved in thymocyte apoptosis through internucleosomal DNA fragmentation in concert with a second signal, the activation of protein kinase C.