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Redox signaling in acute oxygen sensing.

Lin Gao1, Patricia González-Rodríguez1, Patricia Ortega-Sáenz1

  • 1Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, Spain; Departamento de Fisiología Médica y Biofísica, Facultad de Medicina, Universidad de Sevilla, Seville, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Seville, Spain.

Redox Biology
|May 6, 2017
PubMed
Summary

Acute oxygen sensing by the carotid body is vital for survival. Ablating the Ndufs2 gene in mitochondria specifically blocks this oxygen response, revealing key signaling roles for reactive oxygen species and NADH.

Keywords:
Acute oxygen sensingAdrenal medullaCarotid bodyHypoxiaMitochondrial complex IPeripheral chemoreceptorsPyridine nucleotidesReactive oxygen species (ROS)

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Area of Science:

  • Physiology
  • Cell Biology
  • Neuroscience

Background:

  • Acute oxygen (O2) sensing is critical for survival during hypoxia.
  • The carotid body (CB) contains O2-sensitive glomus cells that regulate breathing.
  • The precise molecular mechanisms of O2 sensing in glomus cells remain unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms of O2 sensing in carotid body glomus cells.
  • To identify the role of mitochondrial function in O2 chemoreception.

Main Methods:

  • Selective ablation of the mitochondrial Ndufs2 gene in glomus cells.
  • Assessment of glomus cell responses to hypoxia, hypercapnia, and hypoglycemia.
  • Analysis of potential signaling molecules like reactive oxygen species and NADH.

Main Results:

  • Ablation of the Ndufs2 gene specifically abolished hypoxia-induced O2 sensitivity in glomus cells.
  • Responsiveness to hypercapnia and hypoglycemia remained intact after Ndufs2 gene ablation.
  • Data suggest mitochondrial complex I-generated reactive oxygen species and NADH are key signaling molecules.

Conclusions:

  • Mitochondrial Ndufs2 is essential for acute O2 sensing in the carotid body.
  • Reactive oxygen species and NADH from mitochondrial complex I modulate K+ channels during hypoxia.
  • Proposed 'O2-sensing microdomains' involve mitochondria and plasma membrane K+ channels in glomus cells.