Skip Navigation
Skip to contents

Diabetes Metab J : Diabetes & Metabolism Journal

Search
OPEN ACCESS

Articles

Page Path
HOME > Diabetes Metab J > Volume 30(3); 2006 > Article
Original Article Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.
Eun Hee Koh, Youn Mi Kim, Ha Jung Kim, Woo Je Lee, Jong Chul Won, Min Seon Kim, Ki Up Lee, Joong Yeol Park
Diabetes & Metabolism Journal 2006;30(3):151-160
DOI: https://doi.org/10.4093/jkda.2006.30.3.151
Published online: May 1, 2006
  • 2,273 Views
  • 24 Download
  • 0 Crossref
  • 0 Scopus
1Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Ulsan College of Medicine, Korea.
2Asan Institute for Life Sciences, University of Ulsan College of Medicine, Korea.
prev next

BACKGROUND
Fatty acids contribute to endothelial cell dysfunction and apoptosis by inducing accumulation of long chain fatty acyl CoA (LCAC), which increases oxidative stress in vascular endothelial cells. Forced expression of PGC-1 was shown to induce mitochondrial biogenesis and to control expression of mitochondrial enzymes involved in fatty acid oxidation. This study was undertaken to test the hypothesis that PGC-1 overexpression could prevent endothelial cell apoptosis by enhancing fatty acid oxidation and relieving oxidative stress in vascular endothelium. METHODS: Adenoviruses containing human PGC-1 (Ad-PGC-1) and beta-galactosidase (Ad-beta-gal) were transfected to confluent human aortic endothelial cells (HAECs). To investigate the effect of adenoviral PGC-1 gene transfer on apoptosis, combined treatment of linoleic acid (LA), an unsaturated fatty acid, was performed. RESULTS: PGC-1 overexpression inhibited the increase in ROS production and apoptosis of HAECs induced by LA. Also, PGC-1 led to a significant increase in fatty acid oxidation and decrease in triglyceride content in HAECs. LA caused the decrease of adenine nucleotide translocase (ANT) activity and transient mitochondrial hyperpolarization, which was followed by depolarization. PGC-1 overexpression prevented these processes. CONCLUSION: In summary, PGC-1 overexpression inhibited mitochondrial dysfunction and apoptosis by facilitating fatty acid oxidation and protecting against the damage from oxidative stress in HAECs. The data collectively suggest that the regulation of intracellular PGC-1 expression might play a critical role in preventing atherosclerosis.

  • Cite
    CITE
    export Copy
    Close
    Download Citation
    Download a citation file in RIS format that can be imported by all major citation management software, including EndNote, ProCite, RefWorks, and Reference Manager.

    Format:
    • RIS — For EndNote, ProCite, RefWorks, and most other reference management software
    • BibTeX — For JabRef, BibDesk, and other BibTeX-specific software
    Include:
    • Citation for the content below
    Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.
    Korean Diabetes J. 2006;30(3):151-160.   Published online May 1, 2006
    Close
Related articles
Koh EH, Kim YM, Kim HJ, Lee WJ, Won JC, Kim MS, Lee KU, Park JY. Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.. Diabetes Metab J. 2006;30(3):151-160.
DOI: https://doi.org/10.4093/jkda.2006.30.3.151.

Diabetes Metab J : Diabetes & Metabolism Journal
Close layer
TOP