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First published on March 26, 2007; DOI: 10.1124/mol.106.033845

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Received for publication December 29, 2006.
Revised March 23, 2007.
Accepted for publication March 26, 2007.

The Thiazolidinedione Pioglitazone Alters Mitochondrial Function in Human Neuronal-Like Cells

Sangeeta Ghosh 1, Nishant Patel 1, Douglas Rahn 1, Jenna McAllister 1, Sina Sadeghi 2, Geoffrey Horwitz 1, Diana Berry 1, Kai Xuan Wang 1, Russell H. Swerdlow 1*

1 University of Virginia 2 University of Virginia,

* Address correspondence to: E-mail: rhs7e{at}virginia.edu

Abstract

Thiazolidinediones alter cell energy metabolism. They are used to treat or are being considered for the treatment of disorders that feature mitochondrial impairment. Their mitochondrial effects, though, have not been comprehensively studied under chronic exposure conditions. We used the human neuronal-like NT2 cell line to directly assess the chronic effects of a thiazolidinedione drug, pioglitazone, on mitochondria. At micromolar concentrations, pioglitazone increased mitochondrial DNA (mtDNA) content, levels of mtDNA and nuclear-encoded electron transport chain subunit proteins, increased oxygen consumption, and elevated complex I and complex IV Vmax activities. Pioglitazone treatment was also associated with increased cytoplasmic but reduced mitochondrial peroxide levels. Our data suggest pioglitazone induces mitochondrial biogenesis and show pioglitazone reduces mitochondrial oxidative stress in a neuronal-like cell line. For these reasons pioglitazone may prove useful in the treatment of mitochondriopathies.


Key words: PPARs, Mitochondrial toxins, Oxidative stress/antioxidants, Oxidative stress


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