Cited by 266Cancer, Hypoxia, and MetabolismRedox biology and oxidative stressMitochondrial Function and Pathology

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Hypoxic but not anoxic stabilization of HIF-1α requires mitochondrial reactive oxygen species

Schroedl, Clara, McClintock, David S., Budinger, G. R. Scott, Chandel, Navdeep S.·2002·American Journal of Physiology-Lung Cellular and Molecular Physiology

DOI 10.1152/ajplung.00014.2002

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Abstract

The molecular mechanisms by which cells detect hypoxia (1.5% O2), resulting in the stabilization of hypoxia-inducible factor 1alpha (HIF-1alpha) protein remain unclear. One model proposes that mitochondrial generation of reactive oxygen species is required to stabilize HIF-1alpha protein. Primary evidence for this model comes from the observation that cells treated with complex I inhibitors, such as rotenone, or cells that lack mitochondrial DNA (rho(0)-cells) fail to generate reactive oxygen species or stabilize HIF-1alpha protein in response to hypoxia. In the present study, we investigated the role of mitochondria in regulating HIF-1alpha protein stabilization under anoxia (0% O2). Wild-type A549 and HT1080 cells stabilized HIF-1alpha protein in response to hypoxia and anoxia. The rho(0)-A549 cells and rho(0)-HT1080 cells failed to accumulate HIF-1alpha protein in response to hypoxia. However, both rho(0)-A549 and rho(0)-HT1080 were able to stabilize HIF-1alpha protein levels in response to anoxia. Rotenone inhibited hypoxic, but not anoxic, stabilization of HIF-1alpha protein. These results indicate that a functional electron transport chain is required for hypoxic but not anoxic stabilization of HIF-1alpha protein.

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Authors: Schroedl, C., McClintock, D. S., Budinger, G. R. S., & Chandel, N. S.
Affiliations: Northwestern University (US)
ORCID: Schroedl, Clara
McClintock, David S.
Budinger, G. R. Scott
Chandel, Navdeep S.
Venue: American Journal of Physiology-Lung Cellular and Molecular Physiology
Publisher: American Physiological Society
Published: 2002-11-01
Volume: 283
Issue: 5
Pages: L922-L931
ISSN: 1040-0605 (ISSN-L)
1522-1504
DOI: 10.1152/ajplung.00014.2002
OpenAlex: W2095062583
Cited by: 266
References: 39
Citations by year: 2026: 2 · 2025: 3 · 2024: 5 · 2023: 4 · 2022: 6 · 2021: 13 · 2020: 4 · 2019: 9 · 2018: 5 · 2017: 14 · 2016: 9 · 2015: 11 · 2014: 8 · 2013: 14 · 2012: 11
FWCI: 5.72
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of General Medical Sciences (R01GM060472, GM60472-03)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: HIF-1α stabilization, hypoxia, anoxia, mitochondrial reactive oxygen species, electron transport chain, rotenone, mitochondrial DNA deletions, mitochondrial complex I inhibition, A549 cells, HT1080 cells
MeSH terms: Adenosine Triphosphate, Animals, Hypoxia, Cell Line, Cricetinae, Humans, Kinetics, Lung, Mitochondria, Oxygen Consumption, Recombinant Proteins, Transcription Factors, Transfection, Cell Hypoxia, Apoptosis, Reactive Oxygen Species, Genes, Reporter, Urothelium, Respiratory Mucosa, Hypoxia-Inducible Factor 1, alpha Subunit

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Hypoxic but not anoxic stabilization of HIF-1α requires mitochondrial reactive oxygen species

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