This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Estrogen has been shown to play a protective role in cardiac hypertrophy and heart failure in both humans and rodent models. My current working hypothesis is that male/female differences in susceptibility to systolic LV dysfunction in the setting of cardiac hypertrophy is due to regulation of miRNAs by estrogens. During the first year, I have completed Specific Aim 1 by characterizing pressure overload induced cardiac remodeling in female C57BL6 and 129SvImJ mice. This work was published in collaboration with my mentor, Dr. Susan Smyth, in the American Journal of Physiology [unreadable]Heart Circulation Physiology in Sept 2009. Our work has demonstrated that female C57BL6 are relatively protected in terms of cardiac remodeling and function in response to pressure overload. Our work further showed that there is no male susceptibility gene present on the Y chromosome, thus further supporting the presence of a female "factor", provides the protection from cardiac hypertrophy and heart failure. In addition, during my first year of KBRIN funding I was able to establish a rodent wing of our current animal care facility, including the appropriate IACUC protocol approval. I am now able to do the rat experiments at my home institution, Eastern Kentucky University. During year 2 I will work to accomplish the remaining 2 aims: I have Aim 2) to establish separate miRNA profiles for males and females cardiac remodeling following pressure overload. Aim 3) to determine which miRNAs play a functional role in estrogen mediated inhibition of cardiomyocyte hypertrophy.