A Computational analysis of cardiac aging using mRNA and protein expression data.

Document Type


Publication Date

Summer 2018

JAX Location

In: Student Reports, Summer 2018, The Jackson Laboratory


The aging cell has been associated with dysfunctions in protein homeostasis even when disease is not present (de Magalhaes). The aging cardiac proteome, like other aging cellular proteomes, displays increased protein oxidation and damage, increased ubiquitination, and dysfunction of the autophagy and ubiquitin quality control systems (Rabinovitch). The goal of this project was to make a pipeline that would further elucidate how genetic variation affects the aging heart using transcriptome and proteome wide heart expression data. We hypothesized that proteins forming the quality control systems in the heart would become less expressed in age. We found several genomic hotspots associated with different processes and changes in mRNA and protein expression levels. We suspect lincRNAs, which lie under many of the hotspots, to be the mediators of many of these associations. Of particular interest was a genomic location on chromosome 3 at 147.5 Mbp that was associated with the decline in expression of structural heart proteins with age. We also found that correlations between mRNA and their respective proteins decreases with age, but the way in which the decrease occurs is sex-dependent.

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