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Requirement of nitric oxide and calcium mobilization for the induction of apoptosis in adrenal vascular endothelial cells
Author(s) -
López-Collazo Eduardo,
Mateo Jesús,
Miras-Portugal Marı́a T,
Boscá Lisardo
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)00893-4
Subject(s) - apoptosis , nitric oxide , intracellular , microbiology and biotechnology , lipopolysaccharide , calcium in biology , dna laddering , endothelial stem cell , ex vivo , tumor necrosis factor alpha , programmed cell death , chemistry , biology , immunology , dna fragmentation , endocrinology , biochemistry , in vitro
Exposure of adrenal vascular endothelial cells (AVEC) to pharmacological nitric oxide (NO) donors, pro‐inflammatory cytokines or lipopolysaccharide was unable to induce apoptosis as occurred when macrophages were treated under identical experimental conditions. However, when the intracellular Ca 2+ concentration increased, AVEC displayed apoptotic features upon exposure to NO. This apoptosis was confirmed by the release of oligonucleosomes to the cytosol and by the characteristic DNA laddering observed after electrophoresis in agarose gels. Ca 2+ ‐mobilizing agents and interleukin‐1β (IL‐1β) also elicited an apoptotic response in these cells through a mechanism that required NO synthesis. The ability of NO and intracellular Ca 2+ to promote apoptosis was dependent on the number of passages of the cells in culture, suggesting the loss of protective factors in the course of ex vivo cell culture. Because AVEC exhibit an important capacity to increase the intracellular Ca 2+ concentration in response to a wide array of agonists, this condition might affect the integrity of the vascular system under pathological circumstances such as those prevailing in the course of septic shock.