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Division of Cardiovascular Pathology

Email mhalush1@jhmi.edu
Phone (410) 614-8138
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Marc K. Halushka, M.D., Ph.D.

Primary Appointment in Pathology

MicroRNAs are key post-translational regulators of genes. We are interested in the distribution of microRNAs in human tissues and cells. We are also interested in determining how these microRNAs are altered in human diseases. My laboratory is also involved in a number of collaborative projects relating to cardiovascular diseases such as sudden cardiac death, cardiac citrullination and neonatal lupus.

McCall MN, Kent OA, Yu J, Fox-Talbot K, Zaiman AL, Halushka MK. MicroRNA profiling of diverse endothelial cell types. BMC Med Genomics, 4(1):78, 2011.

Gupta S*, Halushka MK*, Hilton GM, Arking DE. Postmortem cardiac tissue maintains gene expression profile even after late harvesting. BMC Genomics, 13(1):26, 2012.

Giles JT, Fert-Bober J, Park JK, Bingham CO 3rd, Andrade F, Fox-Talbot K, Pappas D, Rosen A, van Eyk J, Bathon JM, Halushka MK. Myocardial citrullination in rheumatoid arthritis: a correlative histopathologic study.. Arth Res Ther. 14(1):R39, 2012.

Kent OA, Fox-Talbot K, Halushka MK. RREB1 repressed miR-143/145 modulates KRAS signaling through down regulation of multiple targets. In Press Oncogene, 2012.

Maleszewski JJ, Murray DL, Dispenzieri A, Grogan M, Judge DP, Caturegli P, Vrana JA, Theis JD, Dogan A, Halushka MK. Relationship between monoclonal gammopathy and cardiac amyloid type. Cardiovasc Pathol, In Press 2012.

Email csteenb1@jhmi.edu
Phone (410) 502-5982
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Charles J. Steenbergen, M.D., Ph.D.

Primary Appointment in Pathology

My research is on mechanisms of ischemic heart disease, and in particular, endogenous mechanisms that can be activated to protect the heart during episodes of ischemia and reperfusion. I am interested in identifying signal transduction pathways that are involved in cardioprotection, and understanding how these signaling pathways confer their protective effect. Recently, we have become interested in how microRNA can regulate mitochondrial protein synthesis and alter mitochondrial function, and we have worked on novel methods for measuring S-nitrosylation, a form of post-translational protein modification that is important in heart disease, and is usually cardioprotective. We hope that better understanding of these mechanisms will lead to the development of better therapies for patients with coronary artery disease, heart failure, and patients undergoing heart surgery.

Murphy, E. and Steenbergen, C.: Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol. Rev. 2008; 88: 581-609.

Das, S., Ferlito, M., Kent, O.A., Fox-Talbot, K., Wang, R., Liu, D., Raghavachari, N., Yang, Y., Wheelan, S.J., Murphy, E., Steenbergen, C. Nuclear miRNA regulates the mitochondrial genome in the heart. Circ. Res. 2012; 110: 1596-1603.

Yano, T., Ferlito, M., Aponte, A., Kuno, A., Miura, T., Murphy, E., Steenbergen, C. Pivotal role of mTORC2 and involvement of ribosomal protein S6 in cardioprotective signaling. Circ. Res. 2014; 114: 1268-1280.

Kohr, M.J., Murphy, E., Steenbergen, C. Glyceraldehyde-3-phosphate dehydrogenase acts as a mitochondrial trans-S-nitrosylase in the heart. PLoS One. 2014; 9: e111448.

Sun, J., Nguyen, T., Aponte, A.M., Menazza, S., Kohr, M.J., Roth, D. M. Patel, H.H., Murphy, E., Steenbergen, C. Ischemic preconditioning preferentially increases protein S-nitrosylation in subsarcolemmal mitochondria. Cardiovasc. Res. 2015; 106: 227-236.


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