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Boosting Mitochondrial Biogenesis Diminishes Foam Cell Formation in the Post-Stroke Brain
Sanna H Loppi1, Marco A Tavera-Garcia1, Natalie E Scholpa2
1Department of Immunobiology, College of Medicine, University of Arizona, Tucson, AZ 85719, USA.
Abstract:
Following ischemic stroke, the degradation of myelin and other cellular membranes surpasses the lipid-processing capabilities of resident microglia and infiltrating macrophages. This imbalance leads to foam cell formation in the infarct and areas of secondary neurodegeneration, instigating sustained inflammation and furthering neurological damage. Given that mitochondria are the primary sites of fatty acid metabolism, augmenting mitochondrial biogenesis (MB) may enhance lipid processing, curtailing foam cell formation and post-stroke chronic inflammation. Previous studies have shown that the pharmacological activation of the β2-adrenergic receptor (β2-AR) stimulates MB. Consequently, our study sought to discern the effects of intensified β2-AR signaling on MB, the processing of brain lipid debris, and neurological outcome using a mouse stroke model. To achieve this goal, aged mice were treated with formoterol, a long-acting β2-AR agonist, daily for two and eight weeks following stroke. Formoterol increased MB in the infarct region, modified fatty acid metabolism, and reduced foam cell formation. However, it did not reduce markers of post-stroke neurodegeneration or improve recovery. Although our findings indicate that enhancing MB in myeloid cells can aid in the processing of brain lipid debris after stroke, it is important to note that boosting MB alone may not be sufficient to significantly impact stroke recovery.
Insights
Enhancing mitochondrial biogenesis (MB) after ischemic stroke helps process lipid debris and reduce foam cells. However, boosting MB alone did not improve neurodegeneration or stroke recovery in aged mice.
Area of Science:
- Neuroscience
- Cellular Biology
- Pharmacology
Background:
- Ischemic stroke causes myelin degradation, overwhelming lipid processing by microglia and macrophages, leading to foam cells and neurodegeneration.
- Mitochondria are key in fatty acid metabolism; enhancing mitochondrial biogenesis (MB) may improve lipid processing and reduce inflammation post-stroke.
- Beta-2 adrenergic receptor (β2-AR) activation is known to stimulate MB.
Purpose of the Study:
- To investigate the effects of enhanced β2-AR signaling on MB, brain lipid debris processing, and neurological outcomes in a mouse stroke model.
- To determine if formoterol, a β2-AR agonist, can mitigate foam cell formation and secondary neurodegeneration after ischemic stroke.
Main Methods:
- Aged mice were subjected to an ischemic stroke model.
- Mice received daily formoterol treatments for two and eight weeks post-stroke.
- Mitochondrial biogenesis, fatty acid metabolism, foam cell formation, and neurodegeneration markers were assessed.
Main Results:
- Formoterol treatment increased mitochondrial biogenesis in the infarct region.
- Enhanced β2-AR signaling modified fatty acid metabolism and reduced foam cell formation.
- No significant reduction in post-stroke neurodegeneration markers or improvement in neurological recovery was observed.
Conclusions:
- Augmenting mitochondrial biogenesis in myeloid cells aids in processing brain lipid debris following ischemic stroke.
- Boosting mitochondrial biogenesis alone may not be sufficient to significantly impact stroke recovery or reduce neurodegeneration.
- Targeting lipid processing pathways warrants further investigation for stroke therapeutic strategies.
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