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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/143408
Título

Oxygen Sensing by Arterial Chemoreceptors Depends on Mitochondrial Complex I Signaling

AutorFernández Agüera, María Carmen; Gao, Lin; González-Rodríguez, P.; Pintado, C. Oscar; Arias-Mayenco, Ignacio; García-Flores, Paula; García-Pergañeda, A.; Pascual Bravo, Alberto ; Ortega-Sáenz, Patricia; López-Barneo, José
Fecha de publicación3-nov-2015
EditorElsevier
CitaciónCell Metabolism 22(5): 825-837 (2015)
ResumenO2 sensing is essential for mammalian homeostasis. Peripheral chemoreceptors such as the carotid body (CB) contain cells with O2-sensitive K+ channels, which are inhibited by hypoxia to trigger fast adaptive cardiorespiratory reflexes. How variations of O2 tension (PO2) are detected and the mechanisms whereby these changes are conveyed to membrane ion channels have remained elusive. We have studied acute O2 sensing in conditional knockout mice lacking mitochondrial complex I (MCI) genes. We inactivated Ndufs2, which encodes a protein that participates in ubiquinone binding. Ndufs2-null mice lose the hyperventilatory response to hypoxia, although they respond to hypercapnia. Ndufs2-deficient CB cells have normal functions and ATP content but are insensitive to changes in PO2. Our data suggest that chemoreceptor cells have a specialized succinate-dependent metabolism that induces an MCI state during hypoxia, characterized by the production of reactive oxygen species and accumulation of reduced pyridine nucleotides, which signal neighboring K+ channels.
Versión del editorhttp://doi.org/10.1016/j.cmet.2015.09.004
URIhttp://hdl.handle.net/10261/143408
DOI10.1016/j.cmet.2015.09.004
Identificadoresissn: 1550-4131
e-issn: 1932-7420
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