Splenic B lymphocyte programmed cell death is prevented by nitric oxide release through mechanisms involving sustained Bcl-2 levels.

A M Genaro; S Hortelano; A Alvarez; C Martínez; L Boscá

doi:10.1172/JCI117869

Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Madrid, Spain.

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Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Madrid, Spain.

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Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Madrid, Spain.

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Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Madrid, Spain.

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Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Madrid, Spain.

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Published in Volume 95, Issue 4 on April 1, 1995
J Clin Invest. 1995;95(4):1884–1890. https://doi.org/10.1172/JCI117869.
© 1995 The American Society for Clinical Investigation

Published April 1, 1995 - Version history

Incubation of ex vivo cultured mature B cells in the presence of nitric oxide or nitric oxide-donor substances delays programmed cell death as determined by the appearance of DNA laddering in agarose gel electrophoresis or by flow-cytometry analysis of DNA. Nitric oxide also rescues B cells from antigen-induced apoptosis but fails to provide a co-stimulatory signal that converts the signal elicited by the antigen into a proliferative response. The protective effects of nitric oxide against programmed cell death can be reproduced by treatment of the cells with permeant analogues of cyclic GMP. Regarding the mechanisms by which nitric oxide prevents apoptosis in B cells, we have observed that nitric oxide release prevents the drop in the expression of the protooncogene bcl-2, both at the mRNA and protein levels, suggesting the existence of an unknown pathway that links nitric oxide signaling with Bcl-2 expression.

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