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TGF-β suppresses the expression of genes related to mitochondrial function in lung A549 cells
Corresponding Author(s) : E. J. Sohn
eunjungs93@gmail.com
Cellular and Molecular Biology,
Vol. 58 No. 2: General Papers
Abstract
TGF-β is a mediator of lung fibrosis and regulates the alveolar epithelial type II cell phenotype. TGF-β can induce epithelial mesenchymal transition of idiopathic pulmonary disease and cancer metastasis. Peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1 α) is a key metabolic regulator that stimulates mitochondrial biogenesis and promotes remodeling of muscle tissue to oxidative fiber-type composition. Here, we report that the induction of TGF-β decreased mRNA expression of PGC-1α, and PGC-1 target genes, such as the transcription factors NRF-2, ERR-α, and PPAR-γ in lung epithelial A549 cells. In addition, TGF-β led to the reduction of super oxide dismutase 2 (anti-oxidant enzyme), cytochrome C (electron transport chain in mitochondria), and MCAD (a mitochondrial β-oxidant enzyme) in A549 cells. Together, our results suggest that TGF-β may suppress the transcriptional activity of the genes related to mitochondrial biogenesis or function. This mechanism may provide a novel insight into the understanding of fibrosis disease.
Keywords
TGF-β
PGC-1α
mitochondrial biogenesis.
Sohn, E. J., Kim, J., Hwang, Y., Im, S., Moon, Y., & Kang, D. M. (2012). TGF-β suppresses the expression of genes related to mitochondrial function in lung A549 cells. Cellular and Molecular Biology, 58(2), 1763–67. Retrieved from http://mail.cellmolbiol.org/index.php/CMB/article/view/562
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