Cardiac hypertrophy is identified on the basis of increased organ size, wall thickness, or cardiac myocyte size. Hypertrophy is the heart’s primary response to physiologic or pathologic increase in work load as virtually all cardiac myocytes are terminally differentiated, thus precluding a hyperplastic response. Conventionally, cardiac hypertrophy has been judged to be a compensatory response to cell injury or increased work load, however sustained hypertrophy is known to be associated with increased morbidity and mortality from cardiovascular disease.

While there has been great progress in identifying various pathways that may contribute to cardiac hypertrophy, we have limited understanding of the factors that contribute to the transition from compensatory hypertrophy to cardiac failure. In a well established model of pressure overload hypertrophy, collaborators have shown that there is an increase in microtubule density in cardiac myocytes. In addition, there is increased expression of microtubule associated protein-4 (MAP4) on the microtubules. We hypothesize that microtubule associated mRNA transport may be impaired in these cells and limit local protein expression and ultimately cardiac hypertrophy. Current work in the lab focuses on the microinjection of fluorescently labeled mRNA transcripts into the nucleus of isolated cardiac myocytes with subsequent real time imaging to determine transport dynamics in control and hypertrophied cells.