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 School 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. β-agonist-mediated relaxation of airway smooth muscle is protein kinase A-dependent
  2. Far from "disappointing"
  3. Exploiting functional domains of GRK2/3 to alter the competitive balance of pro- and anticontractile signaling in airway smooth muscle
  4. Crosstalk between beta-2-adrenoceptor and muscarinic acetylcholine receptors in the airway
  5. GPCRs and arrestins in Airways: Implications for asthma
  6. cAMP regulation of airway smooth muscle function
  7. A-kinase anchoring proteins regulate compartmentalized cAMP signaling in airway smooth muscle
  8. The GPCR OGR1 (GPR68) mediates diverse signalling and contraction of airway smooth muscle in response to small reductions in extracellular pH
  9. β 2-adrenergic receptor agonists modulate human airway smooth muscle cell migration via vasodilator-stimulated phosphoprotein
  10. pH-dependent regulation of the α-subunit of H +-K +-ATPase (HK α2)
  11. New perspectives regarding β 2-adrenoceptor ligands in the treatment of asthma
  12. Anti-mitogenic effects of β-agonists and PGE2on airway smooth muscle are PKA dependent
  13. Deletion of the pH sensor GPR4 decreases renal acid excretion
  14. Asthma and gender impact accumulation of T cell subtypes
  15. Regulation of T cells in airway disease by beta-agonist
  16. Glucocorticoid- and protein kinase A-dependent transcriptome regulation in airway smooth muscle
  17. Agonizing over agonism: Should asthmatics turn their β-receptors on or off?
  18. Endogenous Gs-coupled receptors in smooth muscle exhibit differential susceptibility to GRK2/3-mediated desensitization
  19. Embracing emerging paradigms of G protein-coupled receptor agonism and signaling to address airway smooth muscle pathobiology in asthma
  20. β-Arrestins specifically constrain β2-adrenergic receptor signaling and function in airway smooth muscle