Depletion of Mitochondrial DNA Stabilizes C1qTNF-Related Protein 6 mRNA in Muscle Cells.
10.3346/jkms.2012.27.5.465
- Author:
Mi Jin KIM
1
;
Wan LEE
;
Eun Ju PARK
;
Seung Yoon PARK
Author Information
1. Department of Biochemistry, Dongguk University School of Medicine, Gyeongju, Korea. psyoon@dongguk.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
DNA, Mitochondrial;
CTRP6;
C1qTNF-6;
mRNA Stability;
C2C12 Cells
- MeSH:
Adiponectin/*genetics/metabolism;
Animals;
Cell Line;
DNA, Mitochondrial/*metabolism;
Mice;
Promoter Regions, Genetic;
RNA Stability;
RNA, Messenger/*metabolism;
Up-Regulation
- From:Journal of Korean Medical Science
2012;27(5):465-470
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
