Philadelphia University + Thomas Jefferson University
Sidney Kimmel Medical College
Department of Medicine

Penn, Raymond B.

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Raymond B. Penn

Raymond B. Penn, PhD

Contact Dr. Penn

1020 Locust Street
Suite 543C
Philadelphia, PA 19107

(215) 955-9982
(215) 503-5731 fax


PhD Physiology, Temple University College of Medicine 1988
MS Ed Education, University of Pennsylvania 1980
BA History, University of Pennsylvania 1980

University Appointment

Professor of Medicine
Director, Center for Translational Medicine
Director of Pulmonary Research, Jefferson - Jane and Leonard Korman Lung Center

Professional Societies

American Thoracic Society
American Chemical Society
British Pharmacological 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.


Most Recent Peer-Reviewed Publications

  1. Bronchoprotection and bronchorelaxation in asthma: New targets, and new ways to target the old ones
  2. Phosphodiesterase 4 inhibitors attenuate the asthma phenotype produced by β2-adrenoceptor agonists in phenylethanolamine N-methyltransferase-knockout mice
  3. β2 Agonists
  4. Specificity of arrestin subtypes in regulating airway smooth muscle G protein-coupled receptor signaling and function
  5. Calcilytics for asthma relief
  6. β-agonist-mediated relaxation of airway smooth muscle is protein kinase A-dependent
  7. Far from "disappointing"
  8. Crosstalk between beta-2-adrenoceptor and muscarinic acetylcholine receptors in the airway
  9. GPCRs and arrestins in Airways: Implications for asthma
  10. GPCRs and arrestins in Airways: Implications for asthma
  11. Exploiting functional domains of GRK2/3 to alter the competitive balance of pro- and anticontractile signaling in airway smooth muscle
  12. cAMP regulation of airway smooth muscle function
  13. A-kinase anchoring proteins regulate compartmentalized cAMP signaling in airway smooth muscle
  14. The GPCR OGR1 (GPR68) mediates diverse signalling and contraction of airway smooth muscle in response to small reductions in extracellular pH
  15. β 2-adrenergic receptor agonists modulate human airway smooth muscle cell migration via vasodilator-stimulated phosphoprotein
  16. pH-dependent regulation of the α-subunit of H +-K +-ATPase (HK α2)
  17. New perspectives regarding β 2-adrenoceptor ligands in the treatment of asthma
  18. Anti-mitogenic effects of β-agonists and PGE2on airway smooth muscle are PKA dependent
  19. Asthma and gender impact accumulation of T cell subtypes
  20. Regulation of T cells in airway disease by beta-agonist