PhD, Physiology, Temple University College of Medicine - 1988
MS, Ed Education, University of Pennsylvania - 1980
BA. History, University of Pennsylvania - 1980
Raymond B. Penn, PhD
Professor of Medicine
Director, Center for Translational Medicine
Robley Dunglison Professor of Pulmonary Research
Vice Chair of Research, Department of Medicine
Director of Pulmonary Research, Jane & Leonard Korman Respiratory Institute at Thomas Jefferson University
Contact Information
1020 Locust Street
Jefferson Alumni Hall, Room 543
Philadelphia, PA 19107
215-955-9982
215-503-5731 fax
Professor of Medicine
Director, Center for Translational Medicine
Robley Dunglison Professor of Pulmonary Research
Vice Chair of Research, Department of Medicine
Director of Pulmonary Research, Jane & Leonard Korman Respiratory Institute at Thomas Jefferson University
Education
Publications
- Ovarian Cancer G protein-coupled receptor-1 signaling bias dictates anti-contractile effect of benzodiazepines on airway smooth muscle
- Channeling Relaxation through Multiple Means: TMEM16A Antagonism for Asthma
- A-Kinase–Anchoring Protein Subtypes Differentially Regulate GPCR Signaling and Function in Human Airway Smooth Muscle
- Molecular mechanism of bitter taste receptor agonist-mediated relaxation of airway smooth muscle
- Nestin drives allergen-induced airway smooth muscle hyperplasia and airway remodeling
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..