The Journal of General Physiology
Cell MicroControls
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Published online 11 September 2006 doi:10.1085/jgp.200609591
The Rockefeller University Press, 0022-1295 $8.00
JGP, Volume 128, Number 4, 405-411
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ARTICLE

 Acute Oxygen Sensing in Heme Oxygenase-2 Null Mice



Patricia Ortega-Sáenz, Alberto Pascual, Raquel Gómez-Díaz, and José López-Barneo

Laboratorio de Investigaciones Biomédicas, Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Sevilla 41013, Spain

Correspondence to José López-Barneo: jose.l.barneo.sspa{at}juntadeandalucia.es

Hemeoxygenase-2 (HO-2) is an antioxidant enzyme that can modulate recombinant maxi-K+ channels and has been proposed to be the acute O2 sensor in the carotid body (CB). We have tested the physiological contribution of this enzyme to O2 sensing using HO-2 null mice. HO-2 deficiency leads to a CB phenotype characterized by organ growth and alteration in the expression of stress-dependent genes, including the maxi-K+ channel {alpha}-subunit. However, sensitivity to hypoxia of CB is remarkably similar in HO-2 null animals and their control littermates. Moreover, the response to hypoxia in mouse and rat CB cells was maintained after blockade of maxi-K+ channels with iberiotoxin. Hypoxia responsiveness of the adrenal medulla (AM) (another acutely responding O2-sensitive organ) was also unaltered by HO-2 deficiency. Our data suggest that redox disregulation resulting from HO-2 deficiency affects maxi-K+ channel gene expression but it does not alter the intrinsic O2 sensitivity of CB or AM cells. Therefore, HO-2 is not a universally used acute O2 sensor.

P. Ortega-Sáenz and A. Pascual contributed equally to this work.

Abbreviations used in this paper: AM, adrenal medulla; CB, carotid body; HO-2, hemeoxygenase-2; TH, tyrosine hydroxylase.


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