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Start Over Author "Szweda, Luke I." Journal journal of biological chemistry
15 results on '"Szweda, Luke I."'

11. High Molecular Weight Neurofilament Proteins Are Physiological Substrates of Adduction by the Lipid Peroxidation Product Hydroxynonenal

Author

Wataya, Takafumi, primary, Nunomura, Akihiko, additional, Smith, Mark A., additional, Siedlak, Sandra L., additional, Harris, Peggy L.R., additional, Shimohama, Shun, additional, Szweda, Luke I., additional, Kaminski, Matthew A., additional, Avila, Jesús, additional, Price, Donald L., additional, Cleveland, Don W., additional, Sayre, Lawrence M., additional, and Perry, George, additional

Published
2002
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15. Hypoxia-inducible Factor 2α Regulates Expression of the MitochondrialAconitase Chaperone Protein Frataxin.

Author

Oktay, Yavuz, Dioum, Elhadji, Matsuzaki, Satoshi, Kan Ding, Liang-Jun Yan, Haller, Ronald G., Szweda, Luke I., and Garcia, Joseph A.

Subjects
*PROTEINS, *HYPOXEMIA, *MITOCHONDRIA, *MOLECULAR chaperones, *MANGANESE oxides, *SUPEROXIDE dismutase
Abstract

Mice lacking Epas1, encoding the transcription factor Hypoxia-inducible Factor 2α (HIF-2a), exhibit an apparent mitochon- drial disease state. Similarities between knock-outs of Epasi and of Sod2, encoding the mitochondrial antioxidant enzyme man- ganese superoxide dismutase, led to the identification of Sod2 as a HIF-2a target gene. However, Sod2 levels in Epasi " liver are intermediate between that of Sod~'~ and Sod2~ mice, which have subtle or severe phenotypes, respectively. This suggests that additional HIF-2a target genes besides Sod2 contribute to the Epasi `~ mitochondrial disease state. To define the nature of the mitochondrial defect in Epas1~' liver, we performed biophysical, biochemical, and molecular studies. In the setting of decreased Sod2 levels and increased oxidative stress, we found reduced respiration, sensitized mitochondrial permeabil- ity transition pore opening, intact electron transport chain activi- ties, and impaired mitochondrial aconitase activity. Mitochondrial aconitase protein levels were preserved, whereas mRNA and pro- tein levels for frataxin, the oxidative stress-regulated mitochon- drial aconitase chaperone protein, were markedly reduced in Epasi " livers. The mouse Fxn promoter was preferentially acti- vated by HIF-2a through a consensus HIF-responsive enhancer element. In summary, the studies reveal that Fxn, like Sod2, is a nuclear-encoded, mitochondrial-localized HIF-2a target gene required for optimal mitochondrial homeostasis. These findings expand upon the previously defined role of HIF-2a in the cellular response to oxidative stress and identify a novel link ofHIF-2a with mitochondrial homeostasis. [ABSTRACT FROM AUTHOR]

Published
2007
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