Raymond B. Penn, PhD
Professor of Medicine
Director, Center for Translational Medicine
Director of Pulmonary Research, Jane & Leonard Korman Lung Center
Robley Dunglison Professor of Pulmonary Research
Vice Chair of Research, Department of Medicine
Contact
1020 Locust Street
Jefferson Alumni Hall, Room 543
Philadelphia, PA 19107
215-955-9982
215-503-5731 fax
Raymond B. Penn, PhD
Professor of Medicine
Director, Center for Translational Medicine
Director of Pulmonary Research, Jane & Leonard Korman Lung Center
Robley Dunglison Professor of Pulmonary Research
Vice Chair of Research, Department of Medicine
Education
PhD, Physiology, Temple University College of Medicine - 1988
MS, Ed Education, University of Pennsylvania - 1980
BA. History, University of Pennsylvania - 1980
Publications
- Nestin drives allergen-induced airway smooth muscle hyperplasia and airway remodeling
- Reactive Oxygen Species Behaving Badly: Oxidized Phosphatidylcholines Corrupt Ca2 Signaling in Airway Smooth Muscle
- Crosstalk between diacylglycerol kinase and protein kinase A in the regulation of airway smooth muscle cell proliferation
- Prorelaxant E-type Prostanoid Receptors Functionally Partition to Different Procontractile Receptors in Airway Smooth Muscle
- The biased M3 mAChR ligand PD 102807 mediates qualitatively distinct signaling to regulate airway smooth muscle phenotype
Professional Societies
American Thoracic Society
Research & Clinical Interests
- Airway biology
- GPCR biology
- Asthma pharmacology
- Renal transporter biology
- Cancer biology
- Asthma, COPD
- Obstructive and fibrotic lung diseases
- Chronic metabolic acidosis
The major focus of my research is to identify cellular and molecular mechanisms by which G protein-coupled receptors (GPCRs) mediate important functions in airway cells. GPCR signaling regulates contractile function, synthesis and release of autocrine factors, and cell growth/survival in various airway cells, including airway smooth muscle (ASM), airway epithelium, lung fibroblasts, and T lymphocytes. Aberrant GPCR signaling or exaggerated presentation of GPCR stimuli can promote ASM hypercontractility, airway remodeling, and ASM hyperplasia/hypertrophy, all of which contribute to the pathogenesis of asthma and COPD. Moreover, GPCRs appear to mediate important mitogenic and survival signaling pathways in cells comprising the tumor microenvironment- including epithelia, fibroblasts, stem cells, and inflammatory cells- rendering them potentially important therapeutic targets in the treatment of cancer. Finally, many GPCR genes possess mutations that alter their expression or function; we are particularly interested in characterizing such altered function and its contribution to disease state or disease therapy..