Executive Vice President, UPMC
Dr. Shapiro is the Executive Vice President and Chief Medical and Scientific Officer, UPMC and the President of the Physician Services Division. Dr Shapiro obtained BS and MD degrees from the University of Chicago. He completed his internship, medicine residency, chief residency, and pulmonary & critical fellowship all at Barnes-Jewish Hospital of Washington University School of Medicine in St. Louis. He later joined the faculty at Washington University and was appointed Professor of Medicine, Pediatrics, and Cell Biology in 2000. Dr Shapiro relocated to Boston in 2001 to become the Parker B. Francis Professor and Chief of Pulmonary and Critical Care Medicine at Brigham and Women’s Hospital, Harvard Medical School, before leaving for Pittsburgh in 2006.
Dr. Shapiro’s laboratory focuses on the role of inflammatory cell derived proteinases in the progression of COPD/emphysema and lung cancer. He originally cloned and knocked-out macrophage elastase (MMP-12) to demonstrate that MMP-12 deficient mice are completely protected from the development of cigarette smoke-induced emphysema. Dr. Shapiro’s lab has continued to study the contribution of numerous inflammatory cell derived proteinases in emphysema and lung cancer progression using gene targeting in mice. More recently, his lab has begun to study the role of repair (or lack thereof) in the progression of emphysema by using lineage-tagging approaches to study putative stem cell populations residing within the lung.
Shapiro, New Engl. J. Med. 5/05
Inflammatory-Cell Interactions in Chronic Obstructive Pulmonary Disease (COPD) and the Role of Histone Acetylation.
Hypothesized common origins of emphysema and lung cancer.
Under normal conditions, lung homeostasis is preserved via low-level cell turnover with alveolar macrophages patrolling the lower airspace to remove invading pathogens and particles. Upon exposure to cigarette smoke, inflammatory cells, particularly neutrophils and macrophages, are recruited and activated causing them to release serine and matrix metalloproteinases (MMPs) and reactive oxygen species (ROS). Emphysema results when extracellular matrix destruction and cell death exceeds reparative capacity leading to airspace enlargement. BASCs attempt to replace damaged alveolar cells and maintain alveolar integrity. However, repeated induction of BASC proliferation in the context of cigarette carcinogens and inflammatory proteinase-mediated release of growth factors predisposes these cells to become malignant, leading to bronchogenic carcinoma. Houghton et al., Nature Med 14, 1023-1024 (2008).
Houghton AM, Quintero PA, Perkins DL, Kobayashi DK, Kelley DG, Marconcini LA, Mecham RP, Senior RM, Shapiro SD. Elastin fragments drive disease progression in a murine model of emphysema. J Clin Invest. 116, 753-759 (2006).
Belaaouaj A, McCarthy R, Baumann M, Gao Z, Ley TJ, Abraham SN, Shapiro SD. Mice lacking neutrophil elastase reveal impaired host defense against gram negative bacterial sepsis. Nat Med. 4, 615-618 (1998).
Hautamaki RD, Kobayashi DK, Senior RM, Shapiro SD. Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. Science 277, 2004-2004 (1997).
Dr. Shapiro was featured in PittMed magazine in 2007