Glycoxidative stress-induced mitophagy modulates mitochondrial fates

Mei Chen Lo, Chin I. Lu, Ming Hong Chen, Chun Da Chen, Horng Mo Lee, Shu Huei Kao

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Diabetes mellitus (DM), a state of chronic hyperglycemia, is associated with a variety of serious complications. Hyperglycemia-induced advanced glycation end products (AGEs) play an important role in the development of diabetic complications. In vivo, we demonstrated that disrupted mitochondria and autophagy was elevated in type II DM dbdb mice. Mitophagy was evidenced by increased autophagosome formation in the β-islet cells. The adducts of Nε-(carboxymethyl) lysine (CML), a major AGE, and bovine serum albumin (CML-BSA) stimulated the conversion of microtubule-associated protein 1 light chain 3-I (LC3-I) to LC3-II in rat insulinoma cells (RIN-m5F). CML-BSA increased ROS generation as demonstrated in a time-dependent manner. Experiments with mitochondrial targeted enhanced yellow fluorescent protein transfected RIN-m5F cells, massive fragmented mitochondria were visualized in the CML-BSA treated cells. Taken together, these data suggested that AGEs may cause mitochondrial dysfunction and mitophagosome formation, and AGEs-induced glycoxidative stress may trigger mitophagic process to modulate mitochondrial fates leading to either cell survival or cell death.

Original languageEnglish
Pages (from-to)1-7
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1201
DOIs
Publication statusPublished - Jul 2010

Keywords

  • mitochondrial morphology
  • mitophagy I
  • N-(carboxymethyl) lysine
  • reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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