Effects of 10-week treadmill exercise on the improvement of obesity-induced autophagy dysregulation in arterial endothelial cells of mice

Ji Seok Kim, Tae Bong Jeon, Kyung Wan Baek, Jun Il Yoo, Sang Hyun An, Hyo Youl Moon

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

PURPOSE: Impaired autophagy, a conserved process for the cellular energy homeostasis by degrading damaged cytosolic constituents, is an important contributor to the pathogenesis of atherosclerosis. The purpose of this study was to determine whether regular aerobic exercise can improve obesity-induced dysregulation of autophagy in mice arterial endothelial cells. METHODS: High-fat diet-induced obese mice were subjected to the treadmill running for 10 weeks (15 m/min, 1 hour/day, 6 days/ week). Endothelial cells were isolated from aorta by perfusing with QIAzol reagent. The mRNA and protein expressions of autophagy-related genes were investigated by qRT-PCR and western-blot respectively. Statistical analysis was performed by one-way ANOVA. RESULTS: Autophagy-related gene expressions in both levels of mRNA and protein were significantly decreased in vascular endothelial cells and arterial vessels of obese mice. However, these phenomena have been partly reversed by the regular treatment of treadmill exercise for 10 weeks. Furthermore, eNOS downregulation induced by the obesity was also improved by the regular aerobic exercise, representing enhanced endothelial function. CONCLUSIONS: The current study has shown that the obesity-induced autophagy dysregulation and vascular dysfunction can be partly improved by the regular aerobic exercise in mice vascular endothelial cells.

Original languageEnglish
Pages (from-to)263-269
Number of pages7
JournalExercise Science
Volume28
Issue number3
DOIs
StatePublished - Aug 2019
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2019 Korean Society of Exercise Physiology.

Keywords

  • Aerobic exercise
  • Autophagy
  • Obesity
  • Vascular endothelial cells

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