Department of Medicine
University of Pittsburgh
Majd Mouded, MD
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Assistant Professor of Medicine Phone: 412-692-2211 |
Bio
Majd Mouded received his M.D. from Tufts University in 1999 after being accepted into their BA/MD program. He completed his residency in internal medicine at the Johns Hopkins Hospital in Baltimore, MD. He went on to complete a clinical fellowship at the combined Pulmonary/ Critical Care program of Harvard in Boston, MA. Following his clinical training, he joined the laboratory of Dr. Steven D. Shapiro at the Brigham and Women’s Hospital. In August of 2006, he relocated, along with Dr. Shapiro, to the University of Pittsburgh where he joined the faculty in the department of Pulmonary, Allergy and Critical Care as an Instructor of Medicine.
Clinical Interests
Dr Mouded’s clinical interests are bound tightly to COPD which is the main focus of his basic science research. He spends his clinical time in the inpatient setting on the consult service or in the intensive care unit.
Academic and Research Interests
Dr Mouded has focused on two main areas of COPD/ emphysema research; 1) the role of apoptosis in the pathogenesis of emphysema and 2) the role that adult stem cells residing in the airways contribute to the repair of lung parenchyma. His work involves murine models of emphysema using either an elastase model or a direct cigarette smoke exposure model. His research utilizes analysis of whole tissue, protein, DNA, and RNA. Furthermore, recent interests have involved cloning to generate new mouse strains. Below are data showing ongoing projects:
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General Inhibition of apoptosis in an inflammatory model results in worsening of emphysema. The two top panels are given an intratracheal control (PBS) either with an injectable control (vehicle) or with a general caspase/ apoptosis inhibitor (Z-Asp). The bottom panels are treated with elastase (PPE) again either with or without an apoptosis inhibitor. As shown, the emphysema is worse if the animals are treated with an apoptosis inhibitor. Dr Mouded is currently working to determining possible causes of the worsened emphysema. |
One possible cause is that macrophages that take up apoptotic cells behave differently. We have developed methods to apoptose cells and have them taken up by macrophages. MLE cells are a cell line derived from epithelial cells. As shown in the bottom panels, they are readily taken up by macrophages after they apoptose. Dr Mouded is currently evaluating how the uptake of these cells alters their behavior. |
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Different from mesenchymal or bone marrow stem cells, a recent, resident population of adult stem cells has been described that is felt to reside in the airways. It is unclear how they contribute to repair. As shown, the lab has derived a way to tag these cells (blue) and follow them in injury. Dr Mouded is currently determining both quantitatively and qualitatively how these cells may contribute to repair. |
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Key Publications
Fredenburgh LE, Baron RM, Carvajal IM, Mouded M, Macias AA, Ith B, Perrella MA. Absence of heme oxygenase-1 expression in the lung parenchyma exacerbates endotoxin-induced acute lung injury and decreases surfactant protein-b levels. Cellular and molecular biology (Noisy-le-Grand, France) 2005;51:513-520.
Houghton AM, Mouded M, Shapiro SD. Common origins of lung cancer and copd. Nature medicine 2008;14:1023-1024.
Robbins CS, Franco F, Mouded M, Cernadas M, Shapiro SD. Cigarette smoke exposure impairs dendritic cell maturation and t cell proliferation in thoracic lymph nodes of mice. J Immunol 2008;180:6623-6628.