Mitochondria as signaling organelles in the vascular endothelium.
- Resource Type
- Article
- Authors
- Quintero, Marisol; Colombo, Sergio L.; Godfrey, Andrew; Moncada, Salvador
- Source
- Proceedings of the National Academy of Sciences of the United States of America. 4/4/2006, Vol. 103 Issue 14, p5379-5384. 6p.
- Subject
- *MITOCHONDRIA
*VASCULAR endothelium
*ORGANELLES
*ENDOTHELIUM
*VASCULAR smooth muscle
*CELLS
*REACTIVE oxygen species
- Language
- ISSN
- 0027-8424
Vascular endothelial cells are highly glycolytic and consume relatively low amounts of oxygen (O2) compared with other cells. We have confirmed that oxidative phosphorylation is not the main source of ATP generation in these cells. We also show that at a low O2 concentration (<1%) endogenous NO plays a key role in preventing the accumulation of the α-subunit of hypoxia-inducible factor 1. At higher O2 concentrations (1-3%) NO facilitates the production of mitochondrial reactive oxygen species. This production activates the AMP-activated protein kinase by a mechanism independent of nucleotide concentrations. Thus, the primary role of mitochondria in vascular endothelial cells may not be to generate ATP but, under the control of NO, to act as signaling organelles using either O2 or O2-derived species as signaling molecules. Diversion of O2 away from endothelial cell mitochondria by NO might also facilitate oxygenation of vascular smooth muscle cells. [ABSTRACT FROM AUTHOR]