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

Pera, Tonio

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Tonio Pera, PhD

Contact Dr. Pera

1020 Locust Street
Jefferson Alumni Hall, Room 236
Philadelphia, PA 19107

(215) 503-5127
(215) 503-5731 fax

Education
PhD, University of Groningen in the Netherlands 2011

University Appointment
Assistant Professor

Professional Societies
American Thoracic Society

Research and Clinical Interests
Applying novel GPCR biology and pharmacology to diseases involving smooth muscle dysfunction. G protein-coupled receptors (GPCRs) are the largest protein family in the human genome and the majority of most prescribed drugs target GPCRs.  The work in Dr. Pera’s lab combines expertise in physiology and pharmacology with GPCR biology and biochemistry with the goal of identifying GPCR ligands which exploit novel signaling mechanisms to manage smooth muscle function and thereby treat cardiovascular and lung diseases. Drug development for cardiovascular and lung diseases has focused largely on refinement within the existing classes of drugs and on the use of combinations of these drugs. This strategy has led to improvements in disease management, but as various classes of drugs have reached their full potential this strategy will yield diminishing returns. The concept of biased agonism that has emerged recently indicates that certain ligands of GPCRs may not only turn receptors on or off but also induce qualitatively distinct signaling by the receptors. Our research aims to utilize this novel concept of biased agonism to fine-tune receptor signaling so as to eliminate detrimental, and promote beneficial, signaling in the pulmonary and vascular systems. Specifically, our current work involves: 1) identifying arrestin-biased muscarinic ligands and delineating muscarinic arrestin signaling in airway smooth muscle with the goals of treating asthma and COPD; and 2) targeting specific eicosanoid receptors (EP prostaglandin, cysteinyl leukotriene) with novel subtype selective or biased ligands to manage excessive vascular smooth muscle growth that contributes to hypertension, heart attacks, and stroke. 

Publications

Most Recent Peer-Reviewed Publications

  1. Pepducins as a potential treatment strategy for asthma and COPD
  2. Biased signaling of the proton-sensing receptor OGR1 by benzodiazepines
  3. An official American thoracic society research statement: Current challenges facing research and therapeutic advances in airway remodeling
  4. Bronchoprotection and bronchorelaxation in asthma: New targets, and new ways to target the old ones
  5. Phosphodiesterase 4 inhibitors attenuate the asthma phenotype produced by β2-adrenoceptor agonists in phenylethanolamine N-methyltransferase-knockout mice
  6. Antimitogenic effect of bitter taste receptor agonists on airway smooth muscle cells
  7. Specificity of arrestin subtypes in regulating airway smooth muscle G protein-coupled receptor signaling and function
  8. Metformin attenuates hyperoxia-induced lung injury in neonatal rats by reducing the inflammatory response
  9. Crosstalk between beta-2-adrenoceptor and muscarinic acetylcholine receptors in the airway
  10. Arginase inhibition prevents Inflammation and Remodeling in a Guinea Pig model of Chronic obstructive Pulmonary disease
  11. Airway smooth muscle in asthma: Linking contraction and mechanotransduction to disease pathogenesis and remodelling
  12. Exploiting functional domains of GRK2/3 to alter the competitive balance of pro- and anticontractile signaling in airway smooth muscle
  13. Quaking, an RNA-binding protein, is a critical regulator of vascular smooth muscle cell phenotype
  14. Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells
  15. TAK1 plays a major role in growth factor-induced phenotypic modulation of airway smooth muscle
  16. Tiotropium inhibits pulmonary inflammation and remodelling in a guinea pig model of COPD
  17. Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype
  18. Arginase and pulmonary diseases
  19. Pharmacology of airway smooth muscle proliferation