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P35-sensitive caspases, MAP kinases and Rho modulate ß-adrenergic induction of apoptosis in mollusc immune cells

Station Biologique de Roscoff, CNRS, Université Paris VI, INSU Place Georges Teissier, B.P. 74, F-29682 Roscoff cedex, France

^* Author for correspondence (e-mail: lacoste{at}itsa.ucsf.edu )

Accepted 1 November 2001

Apoptosis is an important mechanism for the preservation of a healthy and balanced immune system in vertebrates. Little is known, however, about how apoptotic processes regulate invertebrate immune defenses. In the present study, we show that noradrenaline, a catecholamine produced by the neuroendocrine system and by immune cells in molluscs, is able to induce apoptosis of oyster Crassostrea gigas hemocytes. The apoptosis-inducing effect of noradrenaline was mimicked by isoproterenol and blocked by propranolol, which indicates that noradrenaline triggers apoptosis via a ß-adrenergic signaling pathway. Exposure to the pan-caspase inhibitor Z-VAD-FMK or expression of the caspase inhibitor P35 under the transcriptional control of a mollusc hsp70 gene promoter reduced the number of apoptotic cells among noradrenaline-treated hemocytes. These results suggest that P35-sensitive caspases are involved in the apoptotic process triggered by ß-adrenergic signaling. Complementary experiments suggest that mitogen-activated protein kinases and Rho, a member of the Ras GTPase family, may be involved in antiapoptotic mechanisms that modulate the apoptotic effect of noradrenaline. Taken together, these results provide a first insight into apoptotic processes in mollusc immune cells.

Key words: Mollusc, Immune cell, Noradrenaline, Apoptosis, ß-adrenergic signaling

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