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Endurance Training Protocol and Longitudinal Performance Assays for Drosophila melanogaster
Published on: March 26, 2012
The impact of SPARC on age-related cardiac dysfunction and fibrosis in Drosophila
Leigh Vaughan1, Richard Marley2, Sara Miellet1
1Bournemouth University, Department of Life and Environmental Science, Talbot Campus, Fern Barrow, Poole, Dorset BH12 5BB, UK.
Insights
Cardiac aging in fruit flies shows collagen buildup and reduced heart function. Lowering SPARC levels extended lifespan and improved cardiac health, suggesting conserved aging mechanisms.
Area of Science:
- Cardiovascular Biology
- Aging Research
- Molecular Genetics
Background:
- Tissue fibrosis, characterized by extracellular matrix protein accumulation, is linked to cardiac aging and failure in humans.
- The precise mechanisms of age-related cardiac fibrosis and dysfunction remain incompletely understood.
- Drosophila melanogaster offers a model system to study cardiac aging and collagen deposition.
Purpose of the Study:
- To investigate collagen deposition and cardiac function in aging Drosophila.
- To examine the role of Secreted Protein Acidic and Rich in Cysteine (SPARC) in age-related cardiac fibrosis.
- To determine if Drosophila serves as a relevant model for human cardiac aging.
Main Methods:
- Cardiac function assessed via high-speed videomicroscopy.
- Collagen IV deposition monitored using a fluorescent reporter (Viking gene).
- Pericardin staining used to assess cardiac collagen levels.
- SPARC expression levels manipulated (reduced heterozygosity and overexpression).
Main Results:
- Aging Drosophila hearts showed increased collagen IV and Pericardin deposition, correlating with declined cardiac function.
- SPARC heterozygous flies exhibited extended lifespan and preserved cardiac function with aging.
- Both genotypes showed similar age-related increases in collagen IV and Pericardin.
- SPARC overexpression led to cardiomyopathy and increased Pericardin deposition.
Conclusions:
- The Drosophila heart recapitulates a fibrosis-like phenotype during aging, mirroring human cardiac aging.
- Reduced SPARC expression promotes longevity and cardiac health span in Drosophila without significantly altering collagen accumulation.
- Conserved mechanisms may underlie cardiac fibrosis in humans, with SPARC potentially influencing cardiac aging through pathways beyond gross collagen accumulation.
Abstract:
Tissue fibrosis, an accumulation of extracellular matrix proteins such as collagen, accompanies cardiac ageing in humans and this is linked to an increased risk of cardiac failure. The mechanisms driving age-related tissue fibrosis and cardiac dysfunction are unclear, yet clinically important. Drosophila is amenable to the study of cardiac ageing as well as collagen deposition; however it is unclear whether collagen accumulates in the ageing Drosophila heart. This work examined collagen deposition and cardiac function in ageing Drosophila, in the context of reduced expression of collagen-interacting protein SPARC (Secreted Protein Acidic and Rich in Cysteine) an evolutionarily conserved protein linked with fibrosis. Heart function was measured using high frame rate videomicroscopy. Collagen deposition was monitored using a fluorescently-tagged collagen IV reporter (encoded by the Viking gene) and staining of the cardiac collagen, Pericardin. The Drosophila heart accumulated collagen IV and Pericardin as flies aged. Associated with this was a decline in cardiac function. SPARC heterozygous flies lived longer than controls and showed little to no age-related cardiac dysfunction. As flies of both genotypes aged, cardiac levels of collagen IV (Viking) and Pericardin increased similarly. Over-expression of SPARC caused cardiomyopathy and increased Pericardin deposition. The findings demonstrate that, like humans, the Drosophila heart develops a fibrosis-like phenotype as it ages. Although having no gross impact on collagen accumulation, reduced SPARC expression extended Drosophila lifespan and cardiac health span. It is proposed that cardiac fibrosis in humans may develop due to the activation of conserved mechanisms and that SPARC may mediate cardiac ageing by mechanisms more subtle than gross accumulation of collagen.
