Abstract
Background: microRNAs (miRNAs) have emerged as ideal candidates to regulate the genes involved in tissue homeostasis of the aging heart. Our work suggests a novel role for miR-987 in heart tissue maintenance during aging. Drosophila miR-987 has a highly conserved seed sequence with human miR-95 and miR-545. Both miR-545 and mir-95 have been identified as possible biomarkers in cardiovascular disease and are known to be dysregulated following cardiac events. The physiological consequences of their dysregulation, their molecular mechanism of action and specific gene targets are unknown. Methods and Results: We have characterized the impact of miR-987 loss on homoeostasis of heart morphology and function during aging using a combination of null mutants and heart specific knock down of miR-987 expression. Using SOHA (semi-automated optical heartbeat analysis), we have identified an increase in heart area and diameter around middle age (20 days post eclosion), but no significant change in arrhythmicity index, diastolic interval, systolic interval, and fractional shortening in miR-987 null mutants. We have examined the effect of miR-987 loss on lifespan and found a significant impact on male survival starting at 20 days. Using in silico analysis we have identified multiple (130) human conserved putative miRNA-target gene interactions to further characterize the molecular mechanisms underlying the observed phenotypes. Conclusions: Our results suggest that miR-987 plays and important role in heart tissue homeostasis during aging and may impact the lifespan of mutant animals. The high conservation of Drosophila miR-987 with human miR-95 and miR-545 and their conserved predicted gene targets provides us with an excellent platform to facilitate the discovery of the molecular mechanisms underlying miRNA dysregulation in cardiovascular disease.
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