Literature DB >> 11846408

Lack of contribution of mitochondrial electron transport to acute O(2) sensing in model airway chemoreceptors.

Gavin J Searle1, Matthew E Hartness, Rachel Hoareau, Chris Peers, Paul J Kemp.   

Abstract

We have recently reported that the model airway chemoreceptors, H146 cells, exhibit a significant component of their oxygen-sensing transduction pathway which cannot be explained by activity of NADPH oxidase. Using patch-clamp, we have studied the transduction system linking reduced O(2) to k(+) channel inhibition and report that, in complete contrast to recent suggestions in pulmonary vasculature, O(2) sensing by the model airway chemoreceptors, H146 cells, does not require functional mitochondria. These data show, for the first time, that mitochondrial production of reactive O(2) species is not the unifying mechanism in O(2) sensing. ©2002 Elsevier Science (USA).

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Year:  2002        PMID: 11846408     DOI: 10.1006/bbrc.2002.6428

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  9 in total

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Authors:  Patricia Ortega-Sáenz; Ricardo Pardal; María García-Fernandez; José López-Barneo
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Review 5.  The role of redox changes in oxygen sensing.

Authors:  E Kenneth Weir; Stephen L Archer
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7.  A Fenton reaction at the endoplasmic reticulum is involved in the redox control of hypoxia-inducible gene expression.

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8.  NOX2 (gp91phox) is a predominant O2 sensor in a human airway chemoreceptor cell line: biochemical, molecular, and electrophysiological evidence.

Authors:  Josef Buttigieg; Jie Pan; Herman Yeger; Ernest Cutz
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2012-08-03       Impact factor: 5.464

Review 9.  Hypoxic pulmonary vasoconstriction.

Authors:  J T Sylvester; Larissa A Shimoda; Philip I Aaronson; Jeremy P T Ward
Journal:  Physiol Rev       Date:  2012-01       Impact factor: 46.500

  9 in total

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