Estrogen has been determined to be an influential factor in lessening the harmful effects of cardiac hypertrophy in pre-menopausal women. Myosin heavy chain alpha (MHC-α) is a gene that plays a protective role in the heart. It is up-regulated during adaptive cardiac hypertrophy, allowing the heart to increase in size and beat faster. Levels of thyroid hormone receptor and miRNA 208a expression have been indicated in regulating MHC-α expression levels. By examining estrogen’s metabolic pathway and its effect on MHC-α directly, as well as the effect of MHC protein regulators, the thyroid hormone receptor and thyroid hormone signaling pathway and miRNA 208a, the expression level of MHC-α can be up-regulated in order to treat maladaptive cardiac hypertrophy. RNA was extracted from rat pup cardiomyocytes that were treated with estrogen, estrogen agonist, and estrogen antagonist and run through real-time PCR to determine relative gene expression levels. Analysis of Real Time PCR results showed an increase in expression levels for MHC-α and an increase in expression levels for miRNA 208a using estrogen but a decrease in expression using the antagonist. Results for thyroid hormone receptor were undetermined.

Semester/Year of Award

Spring 2013


Rebekah L. Waikel

Mentor Department Affiliation

Biological Sciences

Access Options

Restricted Access Thesis

Document Type

Bachelor Thesis

Degree Name

Honors Scholars

Degree Level



Biological Sciences

IACUC Approval Number (if applicable)