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Effect of Spermidine on Endothelial Function in Systemic Lupus Erythematosus Mice
Hyoseon Kim1, Michael P Massett1
1Department of Kinesiology and Sport Management, Texas Tech University, Lubbock, TX 79409, USA.
Abstract:
Endothelial dysfunction is common in Systemic Lupus Erythematosus (SLE), even in the absence of cardiovascular disease. Evidence suggests that impaired mitophagy contributes to SLE. Mitochondrial dysfunction is also associated with impaired endothelial function. Spermidine, a natural polyamine, stimulates mitophagy by the PINK1-parkin pathway and counters age-associated endothelial dysfunction. However, the effect of spermidine on mitophagy and vascular function in SLE has not been explored. To address this gap, 9-week-old female lupus-prone (MRL/lpr) and healthy control (MRL/MpJ) mice were randomly assigned to spermidine treatment (lpr_Spermidine and MpJ_Spermidine) for 8 weeks or as control (lpr_Control and MpJ_Control). lpr_Control mice exhibited impaired endothelial function (e.g., decreased relaxation to acetylcholine), increased markers of inflammation, and lower protein content of parkin, a mitophagy marker, in the thoracic aorta. Spermidine treatment prevented endothelial dysfunction in MRL-lpr mice. Furthermore, aortas from lpr_Spermidine mice had lower levels of inflammatory markers and higher levels of parkin. Lupus phenotypes were not affected by spermidine. Collectively, these results demonstrate the beneficial effects of spermidine treatment on endothelial function, inflammation, and mitophagy in SLE mice. These results support future studies of the beneficial effects of spermidine on endothelial dysfunction and cardiovascular disease risk in SLE.
Insights
Spermidine treatment improved vascular function and reduced inflammation in mice with lupus erythematosus (SLE). This natural compound enhanced mitophagy, offering potential benefits for cardiovascular health in SLE patients.
Area of Science:
- Immunology
- Cardiovascular Science
- Mitochondrial Biology
Background:
- Endothelial dysfunction is prevalent in Systemic Lupus Erythematosus (SLE), often preceding cardiovascular disease.
- Impaired mitophagy and mitochondrial dysfunction are implicated in SLE pathogenesis and vascular impairment.
- Spermidine, a natural polyamine, is known to promote mitophagy and improve endothelial function.
Purpose of the Study:
- To investigate the effects of spermidine on mitophagy and vascular function in a mouse model of SLE.
- To determine if spermidine can ameliorate endothelial dysfunction and inflammation associated with SLE.
Main Methods:
- Female lupus-prone (MRL/lpr) and healthy control (MRL/MpJ) mice were treated with spermidine or a control for 8 weeks.
- Endothelial function, inflammatory markers, and mitophagy markers (e.g., parkin) in the thoracic aorta were assessed.
Main Results:
- MRL/lpr mice exhibited impaired endothelial function, increased inflammation, and reduced parkin levels.
- Spermidine treatment prevented endothelial dysfunction in MRL-lpr mice.
- Spermidine administration lowered inflammatory markers and increased parkin levels in SLE mice, without altering lupus phenotypes.
Conclusions:
- Spermidine demonstrates beneficial effects on endothelial function, inflammation, and mitophagy in SLE.
- These findings suggest spermidine as a potential therapeutic agent for cardiovascular complications in SLE.
- Further research is warranted to explore spermidine's role in reducing cardiovascular disease risk in SLE.
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