Kurt Prins, M.D., Ph.D.

Kurt Prins (prin0088@umn.edu) is a cardiologist that focuses on understand pulmonary hypertension and right ventricular dysfunction. His research is translational as he performs both basic science experiments in his NIH-funded laboratory, clinical research, and clinical trials. He has experience with experimental design with both basic and clinical research. His research has been published in high impact journals including: AJRCCM, JACC-Heart Failure, Journal of Heart and Lung Transplantation, JAHA, and JACC-Basic to Translational Research.

Publications:

  1. Prins KW, Rose L, Archer SL, Pritzker M, Weir EK, Kazmirczak F, Misialek JR, Thenappan T. 2018. Disproportionate right ventricular dysfunction and poor survival in group 3 pulmonary hypertension. Am J Physiol Heart Circ Physiol. 197(11):1496-1499.

  2. Prins KW, Archer SL, Pritzker M, Rose L, Weir EK, Sharma A, Thenappan T. Interleukin-6 is Independently Associated with Right Ventricular Dysfunction in Pulmonary Arterial Hypertension. J Heart Lung Transplant. 2018 Mar;37(3):376-384.

  3. Prins KW, Tian L, Wu D, Thenappan T, Metzger JM, Archer SL. Colchicine Depolymerizes Microtubules, Increases Junctophilin-2, and Improves Right Ventricular Function in Experimental Pulmonary Arterial Hypertension. J Am Heart Assoc. 2017 May 31. 6: 1-13.

  4. Prins KW, Duval S, Markowitz J, Pritzker M, Thenappan T. Chronic Effects of PAH-Specific Therapy in World Health Organization Group III Pulmonary Hypertension: A Systematic Review and Meta-Analysis. Pulm Circ. 2017 Mar 24;7(1): 145-155.

  5. Prins KW, Weir EK, Archer SL, Markowitz J, Rose L, Pritzker M, Madlon-Kay R, Thenappan T. Pulmonary Pulse-wave Transit Time is Associated with Right Ventricular-Pulmonary Artery Coupling in Pulmonary Arterial Hypertension. Pulm Circ. 2016 Dec;6(4): 576-585.

  6. Prins KW, Asp ML, Zhang H, Wang W, Metzger JM. Microtubule-mediated Misregulation of Junctophilin-2 Underlies T-tubule Disruptions and Calcium Mishandling in Mdx Mice. JACC Basic Transl Sci. 2016 Apr;1(3): 122-130.

  7. Thenappan T, Prins KW, Pritzker MR, Scandurra J, Volmers K, Weir EK. The Critical Role of Pulmonary Arterial Compliance in Pulmonary Hypertension. Ann Am Thorac Soc. 2016 Feb;13(2): 276-284.

  8. Prins, K.W., J.O. Neill, J.O. Tyler, P.M. Eckman, and S. Duval. Effects of Beta-Blocker Withdrawal in Acute Decompensated Heart Failure: A Systematic Review and Meta-Analysis. JACC Heart Fail. 2015 Aug;3(8): 647-53.

Research Projects Available (Clinical):

  1. Understand the right ventricle in pulmonary hypertension due to lung disease: In this project, we are building on our previous publication (Prins et al., AJRCCM) showing patients with pulmonary hypertension due to chronic lung disease have worse RV function than PAH patients despite having less severe pulmonary vascular disease. We will employ imaging and hemodynamic measures of RV function to gain insight into our observation.

  2. Database analysis to gain insights into PAH pathophysiology: Using the MEASURE database, which has a comprehensive review of over 800 pulmonary hypertension patients, we can perform studies to compare different pulmonary hypertension subgroups or investigate one particular type of pulmonary hypertension.

Research Projects Available (Basic):

  1. Understanding the role of junctophilin-2 in RV failure: In this project, we are building on our previous publication (Prins et al., JAHA) showing junctophilin-2 is downregulated in the RV and associated with t-tubule disruptions and RV dysfunction in rodent PAH. Now, we are looking to define epigenetic regulators of junctophilin-2 and how inhibition of those regulators alters junctophilin-2 protein levels, t-tubule morphology, calcium handling, and RV function in rodent models of PAH.

  2. Investigating the contribution of metabolic derangements to RV failure: Here, we are investigating a novel protein-protein interaction that likely controls RV metabolism through mitochondrial regulation. In this project, we will analyze mitochondrial function and RV metabolism and how altering each modulates RV function in vivo.

  3. Determine the role of inflammation in RV dysfunction: In this project, we are aiming to understand how inflammation may promote impaired RV function. In a clinical study (Prins et al., JHLT), we showed the inflammatory cytokine interleukin-6 was associated with RV failure in PAH patients. The goal of this project is to define the molecular mechanism of this observation in isolated cardiomyocytes and rodent PAH models.