TGF-β SUPPRESSES THE EXPRESSION OF GENES RELATED TO MITOCHONDRIAL FUNCTION IN LUNG A549 CELLS
TGF-β SUPPRESSES THE EXPRESSION OF GENES RELATED TO MITOCHONDRIAL FUNCTION IN LUNG A549 CELLS
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DOI：
10.1170/207
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发表时间：
2012-01-01
影响因子：
1.6
通讯作者：
Kang, D. M.
中科院分区：
文献类型：
--
作者：
Sohn, E. J.;Kim, J.;Kang, D. M.
TGF-beta is a mediator of lung fibrosis and regulates the alveolar epithelial type II cell phenotype. TGF-beta can induce epithelial mesenchymal transition of idiopathic pulmonary disease and cancer metastasis. Peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1 alpha) 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-beta decreased mRNA expression of PGC-1 alpha, and PGC-1 target genes, such as the transcription factors NRF-2, ERR-alpha, and PPAR-gamma in lung epithelial A549 cells. In addition, TGF-beta led to the reduction of super oxide dismutase 2 (anti-oxidant enzyme), cytochrome C (electron transport chain in mitochondria), and MCAD (a mitochondrial beta-oxidant enzyme) in A549 cells. Together, our results suggest that TGF-beta 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.
