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Depletion of Mitochondrial DNA Stabilizes C1qTNF-Related Protein 6 mRNA in Muscle Cells

Mutation and reduction of mitochondrial DNA (mtDNA) have been suggested as factors in the pathogenesis of several metabolic diseases. Recently, we demonstrated that C1qTNF-related protein-6 (CTRP6) is involved in fatty acid metabolism in muscle cells. In this study, we showed that expression of CTRP...

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Detalles Bibliográficos
Autores principales: Kim, Mi-Jin, Lee, Wan, Park, Eun-Ju, Park, Seung-Yoon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Academy of Medical Sciences 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342534/
https://www.ncbi.nlm.nih.gov/pubmed/22563208
http://dx.doi.org/10.3346/jkms.2012.27.5.465
Descripción
Sumario:Mutation and reduction of mitochondrial DNA (mtDNA) have been suggested as factors in the pathogenesis of several metabolic diseases. Recently, we demonstrated that C1qTNF-related protein-6 (CTRP6) is involved in fatty acid metabolism in muscle cells. In this study, we showed that expression of CTRP6 was up-regulated in mtDNA-depleted C2C12 cells, which displayed a marked decrease in cellular mtDNA and ATP content. Replacement of mtDNA normalized the expression level of CTRP6 similar to that in normal C2C12 cells, indicating that CTRP6 expression was up-regulated by mtDNA depletion. However, CTRP6 promoter activity remained unchanged in mtDNA-depleted cells. We also found that mtDNA depletion inhibited decay of CTRP6 mRNA. Taken together, mtDNA depletion induces an increase in CTRP6 expression by increasing mRNA stability.