Susan Marsh
Director of Graduate StudiesClinical Associate Professor, Pharmaceutical Sciences 509-358-7718 PBS 321 Spokane

Education

Ph.D. in human movement studies, The University of Queensland, Brisbane, Australia

Bachelor of Science (Honours I), The University of Queensland, Brisbane, Australia

Bachelor of Health Science, Griffith University, Gold Coast, Australia

Bachelor of Education (Secondary), Queensland University of Technology, Brisbane, Australia

Additional Training

Postdoctoral Scholar, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL

Research Interests

  • Mechanisms of exercise-induced cardioprotection
  • Protein O-GlcNAcylation in the heart
  • Cell signaling events in the heart in response to high fat diets and diabetes

Regular exercise provides protection against cardiovascular disease through a reduction of risk factors such as obesity, hypertension and blood lipids. Acute and short term exercise also provide protection against myocardial infarction (heart attack) by upregulation of protective proteins in heart muscle cells and this is independent of any change in risk factors.

My laboratory investigates the role of post-translational modification of proteins in exercise-induced cardioprotection, in addition to the cardiac response of the O-GlcNAc pathway to high fat diets and diabetes. Experimental techniques include in vivo mouse model (including forced and voluntary exercise training), cell culture, isolated heart perfusion, fluorescent microscopy, western blotting, and PCR.

Selected Publications

Johnson, EJ., Dieter, BP., Marsh, SA. Establishing strategic exercise prescriptions for cardiac hypertrophy: Evidence for distinct effects of exercise in different hypertrophic disorders. Life Sciences. 123: 100–106, 2015. [PMID: 25632833]

Medford, HM., Marsh, SA. The role of O-GlcNAc transferase (OGT) in regulating gene transcription of developing and failing hearts. Future Cardiology. 10(6): 801-812, 2014. [PMID: 25495821]

Marsh, SA., Collins, HE., Chatham, JC. Protein O-GlcNAcylation and Cardiovascular (Patho)physiology. Journal of Biological Chemistry. 89(50): 34449–34456, 2014. [PMID: 25336635]

Rocco, AB., LeValley, JC., Eldridge, JA., Marsh, SA., Rodgers, BD. A novel protocol for assessing exercise performance and dystropathophysiology in the mdx mouse. Muscle & Nerve. 50(4): 541-548, 2014. [PMID: 24449511]

Medford, HM., Cox, EJ., Miller, LE., Marsh, SA. Consuming a Western diet for two weeks suppresses fetal genes in mouse hearts. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. 306(8): R519-26, 2014. [PMID: 24523346]

Cox, EJ., Marsh, SA. A systematic review of fetal genes as biomarkers of cardiac hypertrophy in rodent models of diabetes. PLOS ONE. 9(3): e92903, 2014. [PMID: 24663494]

Cox, EJ., Marsh, SA. Exercise and diabetes have opposite effects on the assembly and O-GlcNAc modification of the mSin3A/HDAC1/2 complex in the heart. Cardiovascular Diabetology. 12: 101, 2013. [PMID: 23835259; PMCID: PMC3708830]

Medford, HM., Porter, K., Marsh, SA. Immediate effects of a single exercise bout on protein O-GlcNAcylation and chromatin regulation of cardiac hypertrophy. American Journal of Physiology – Heart and Circulatory Physiology. 305(1): H114-123, 2013. [PMID: 23624624]

Medford, HM., Chatham, JC., Marsh, SA. Chronic ingestion of a western diet increases O-linked-β-N-acetylglucosamine (O-GlcNAc) protein modification in the heart. Life Sciences. 90(23-24): 883-8, 2012. [PMID: 22575823]

Porter, K., Medford, HM., McIntosh, CM., Marsh, SA. Cardioprotection requires flipping the ‘posttranslational modification’ switch. Life Sciences. 90(3-4): 89-98, 2012. [PMID: 22154907]