Journal
MITOCHONDRION
Volume 11, Issue 1, Pages 76-82Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2010.07.007
Keywords
Mitochondrion; Mitochondrial biogenesis; Mitochondrial respiration; Neuron; Selenoprotein; Cell signaling
Categories
Funding
- National Institute of Health [R01DK075476]
- Golden Leaf Foundation
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK075476] Funding Source: NIH RePORTER
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Overexpression of selenoprotein H (SelH) gene provides neuroprotection in neurons against UVB-induced cell death by blocking the mitochondrial-initiated apoptotic cell death pathway. This study examined the effects of SelH on mitochondrial biogenesis and mitochondrial function. The results demonstrated that overexpression of SelH gene in neuronal HT22 cells significantly increased the levels of mitochondrial biogenesis regulators, nuclear respiratory factor-1 (NRF-1), peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) and mitochondrial transcription factor A (Tfam). Mitochondrial cytochrome c content was elevated, mass was increased and respiration was enhanced. SelH transfection ameliorated ultra violet B (UVB)-induced suppression of mitochondrial biogenesis markers and depolarization of mitochondrial membrane potential. Overexpression of SelH promotes mitochondrial biogenesis and improves mitochondrial functional performance. (C) 2010 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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