Zinc protects chondrocytes from monosodium iodoacetate-induced damage by enhancing ATP and mitophagy

Osteoarthritis (OA) is characterized with articular cartilage degradation, and monosodium iodoacetate (MIA)-treated chondrocyte is the most commonly used model for mimicking OA progression. Zinc protects chondrocytes from MIA-induced damage. Here, we explored the protective effects of 25 μM zinc on...

Full description

Saved in:
Bibliographic Details
Published inBiochemical and biophysical research communications Vol. 521; no. 1; pp. 50 - 56
Main Authors Huang, Li-Wen, Huang, Tzu-Ching, Hu, Yu-Chen, Hsieh, Bau-Shan, Chiu, Pu-Rong, Cheng, Hsiao-Ling, Chang, Kee-Lung
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.01.2020
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Osteoarthritis (OA) is characterized with articular cartilage degradation, and monosodium iodoacetate (MIA)-treated chondrocyte is the most commonly used model for mimicking OA progression. Zinc protects chondrocytes from MIA-induced damage. Here, we explored the protective effects of 25 μM zinc on 5 μM MIA-treated SW1353 cells (human chondrosarcoma cell line) through the analysis of energy metabolism- and autophagy-related parameters. We found that the exposure of SW1353 cells to MIA decreased ATP levels, expression of glycolysis-related proteins, including glucose transporter 1, hexokinase 2, and pyruvate dehydrogenase E1 component subunit alpha, and the levels of mitochondrial complex I, II, IV, and V subunits of the oxidative phosphorylation pathway. MIA treatment also decreased the expression of autophagy-related proteins, including autophagic elongation protein 5 (ATG5), ATG7, and microtubule-associated protein 1A/1B light chain 3B (LC3-II) and mitophagy-related proteins, including phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1), ubiquitin, and p62. These results indicate that MIA interferes with energy metabolism and the autophagic clearance of dysfunctional mitochondria (so called mitophagy). Interestingly, zinc exposure could almost completely reverse the effects of MIA, suggesting its potential protective role against OA progression. [Display omitted] •Zinc increases ATP production.•Zinc enhances autophagy and mitophagy.•Zinc triggers a significant energy metabolism.•Zinc prevents damaged chondrocyte from energy deprived.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2019.10.066