| First Author | Ortega-Sáenz P | Year | 2006 |
| Journal | J Gen Physiol | Volume | 128 |
| Issue | 4 | Pages | 405-11 |
| PubMed ID | 16966473 | Mgi Jnum | J:136743 |
| Mgi Id | MGI:3796926 | Doi | 10.1085/jgp.200609591 |
| Citation | Ortega-Saenz P, et al. (2006) Acute oxygen sensing in heme oxygenase-2 null mice. J Gen Physiol 128(4):405-11 |
| abstractText | Hemeoxygenase-2 (HO-2) is an antioxidant enzyme that can modulate recombinant maxi-K(+) channels and has been proposed to be the acute O(2) sensor in the carotid body (CB). We have tested the physiological contribution of this enzyme to O(2) 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 O(2)-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 O(2) sensitivity of CB or AM cells. Therefore, HO-2 is not a universally used acute O(2) sensor. |
