Exercise training increases CISD family protein expression in murine skeletal muscle and white adipose tissue
Creators
- 1. Laboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto (Japan)
- 2. Faculty of Sport and Health Science, Ritsumeikan University, Kusatsu, Shiga (Japan)
Description
Highlights: • CISD family proteins regulate mitochondrial activity and biogenesis. • We examined the relationship between exercise and CISD expression in muscle and WAT. • Chronic exercise increased CISD1/2 and mitochondrial protein expression in mice. • These increases were observed in plantaris muscle and WAT but not soleus muscle. Mitochondrial function in skeletal muscle and white adipose tissue (WAT) declines with aging and the progression of type 2 diabetes and insulin resistance. Although exercise increases mitochondrial biogenesis and function in both tissues, the molecular mechanisms are not fully understood. CDGSH iron sulfur domain-containing proteins (CISDs) are a novel family of proteins that regulate mitochondrial activity and biogenesis. However, the relationship between exercise and CISD expression is unclear. We addressed this in the present study by examining changes in the expression of CISDs and mitochondrial proteins in skeletal muscle and WAT of mice subjected to chronic exercise training. Mice were randomly assigned to either the sedentary or exercise group and were housed for 4 weeks in a standard cage without or with a running wheel, respectively. CISD and mitochondrial protein levels in the plantaris and soleus muscles and epididymal WAT were evaluated by western blotting. Chronic exercise increased CISD1 and CISD2 as well as mitochondrial protein expression in plantaris muscle and WAT but not soleus muscle. Moreover, this exercise-induced adaptation was strongly correlated with mitochondrial protein expression. Thus, mitochondrial biogenesis induced by chronic exercise coincides with the expression of CISDs in specific tissues, which may be critical for the maintenance of mitochondrial integrity.
Availability note (English)
Available from http://dx.doi.org/10.1016/j.bbrc.2018.10.101Additional details
Identifiers
- DOI
- 10.1016/j.bbrc.2018.10.101;
- PII
- S0006291X18322630;
Publishing Information
- Journal Title
- Biochemical and Biophysical Research Communications
- Journal Volume
- 506
- Journal Issue
- 3
- Journal Page Range
- p. 571-577
- ISSN
- 0006-291X
- CODEN
- BBRCA9
INIS
- Country of Publication
- United States
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 54056579
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- ADIPOSE TISSUE; INSULIN; IRON; MICE; MITOCHONDRIA
- Descriptors DEC
- ANIMAL TISSUES; ANIMALS; BODY; CELL CONSTITUENTS; CONNECTIVE TISSUE; ELEMENTS; HORMONES; MAMMALS; METALS; ORGANIC COMPOUNDS; PEPTIDE HORMONES; PROTEINS; RODENTS; TRANSITION ELEMENTS; VERTEBRATES
Optional Information
- Copyright
- Copyright (c) 2018 The Authors. Published by Elsevier Inc.