Type I cell ROS kinetics under hypoxia in the intact mouse carotid body ex 
vivo: a FRET-based study

Bernardini, A.; Brockmeier, U.; Metzen, E.; Berchner-Pfannschmidt, U.; Harde, E.; Acker-Palmer, Amparo; Papkovsky, D.; Acker, H.; Fandrey, J.

doi:10.1152/ajpcell.00370.2013

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Type I cell ROS kinetics under hypoxia in the intact mouse carotid body ex vivo: a FRET-based study

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Acker-Palmer, Amparo
Neurovascular interface Group, Max Planck Institute for Brain Research, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/25318107
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Citation

Bernardini, A., Brockmeier, U., Metzen, E., Berchner-Pfannschmidt, U., Harde, E., Acker-Palmer, A., et al. (2014). Type I cell ROS kinetics under hypoxia in the intact mouse carotid body ex vivo: a FRET-based study. Am J Physiol Cell Physiol, 308(1), C61-7. doi:10.1152/ajpcell.00370.2013.

Cite as: https://hdl.handle.net/21.11116/0000-0008-0BFC-1

Abstract

Reactive oxygen species (ROS) mainly originating from NADPH oxidases have been shown to be involved in the carotid body (CB) oxygen-sensing cascade. For measuring ROS kinetics, type I cells of the mouse CB in an ex vivo preparation were transfected with the ROS sensor construct FRET-HSP33. After 2 days of tissue culture, type I cells expressed FRET-HSP33 as shown by immunohistochemistry. In one population of CBs, 5 min of hypoxia induced a significant and reversible decrease of type I cell ROS levels (n = 9 CBs; P < 0.015), which could be inhibited by 4-(2-aminoethyl)benzensulfonylfluorid (AEBSF), a highly specific inhibitor of the NADPH oxidase subunits p47(phox) and p67(phox). In another population of CBs, however, 5 min of hypoxia induced a significant and reversible increase of ROS levels in type I cells (n = 8 CBs; P < 0.05), which was slightly enhanced by administration of 3 mM AEBSF. These different ROS kinetics seemed to coincide with different mice breeding conditions. Type I cells of both populations showed a typical hypoxia-induced membrane potential (MP) depolarization, which could be inhibited by 3 mM AEBSF. ROS and MP closely followed the hypoxic decrease in CB tissue oxygen as measured with an O2-sensitive dye. We conclude that attenuated p47(phox) subunit activity of the NADPH oxidase under hypoxia is the physiological trigger for type I cell MP depolarization probably due to ROS decrease, whereas the observed ROS increase has no influence on type I cell MP kinetics under hypoxia.