Department of Medicine
University of Pittsburgh
Michael Myerburg, MD
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Assistant Professor of Medicine Phone: 412-647-8477 |
Bio
Mike Myerburg received his M.D. from the University of Pittsburgh Medical Center in 2000. After his Internal Medicine internship and residency at the University of Pittsburgh, he completed his fellowship in Pulmonary and Critical Care in 2005. He remained in the Pulmonary, Allergy, and Critical Care Medicine Division as a post-doctoral research fellowship, under the mentorship of Joe Pilewski and Tom Kleyman. In July of 2007, he became an Assistant Professor within The Pulmonary, Allergy and Critical Care Medicine Division at the University of Pittsburgh School of Medicine.
Clinical Interests
Dr. Myerburg’s clinical expertise focuses on cystic fibrosis lung disease, general pulmonary medicine, and critical care.
Academic and Research Interests
Dr. Myerburg’s primary research interests include understanding the role of the epithelial sodium channel (ENaC) in cystic fibrosis and other airway diseases. The goal of this research is to delineate how ENaC activity is regulated and to develop novel therapeutic strategies to mitigate sodium hyperabsorption in the airway. Additionally, he is interested in airway epithelial cell biology, as it relates to mucus clearance from the lung and host defense from inhaled pathogens.
Dr. Myerburg has demonstrated (JBC 06) that ENaC is regulated by the relative balance between membrane tethered proteases, which activate the channel, and soluble protease inhibitors that are present in the airway surface liquid. As shown in the schematic below, this “protease – protease inhibitor balance” establishes an auto-regulatory mechanism to maintain optimal airway surface liquid (ASL) hydration.
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Recent work suggests that the balance between channel activating proteases and the endogenous protease inhibitors is altered in cystic fibrosis and related chronic obstructive lung diseases. In particular, we have shown that airway epithelium from cystic fibrosis patients express heightened levels of the protease prostasin (AJP 08). Due to excessive protease activity, ENaC becomes overactive, causing dehydration of the ASL and imparing mucus clearance. |
To study the role of proteases in the physiological regulation of sodium and water absorption in the airway, our lab uses primary human airway epithelium that is cultured from excess pathological tissue following lung transplantation. These primary airway cultures develop into mucus producing layers, with prominent cilia, as shown here. Using this model system, we are able to measure mucus transport, ASL volume and absorption, ciliary beat frequency, and short-circuit current. |
Key Publications
Myerburg MM, Butterworth MB, McKenna EE, Peters KW, Frizzell RA, Kleyman TR, Pilewski JM. Airway surface liquid volume regulates ENaC by altering the serine protease-protease inhibitor balance: a mechanism for sodium hyperabsorption in cystic fibrosis. J Biol Chem. 2006 Sep 22;281(38):27942-9. Epub 2006 Jul 26
Myerburg MM, Latoche JD, McKenna EE, Stabile LP, Siegfried JS, Feghali-Bostwick CA, Pilewski JM. Hepatocyte growth factor and other fibroblast secretions modulate the phenotype of human bronchial epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2007 Jun;292(6):L1352-60. Epub 2007 Feb 16.
Myerburg MM, McKenna EE, Luke CJ, Frizzell RA, Kleyman TR, Pilewski JM. Prostasin expression is regulated by airway surface liquid volume and is increased in cystic fibrosis. Am J Physiol Lung Cell Mol Physiol. 2008 May;294(5):L932-41. Epub 2008 Feb 29.