Tonio Pera, PhD
Assistant Professor
Contact
1020 Locust Street
Jefferson Alumni Hall, Room 236
Philadelphia, PA 19107
215-503-5127
215-503-5731 fax
Tonio Pera, PhD
Assistant Professor
Education
PhD, University of Groningen in the Netherlands - 2011
Publications
- The biased M3 mAChR ligand PD 102807 mediates qualitatively distinct signaling to regulate airway smooth muscle phenotype
- PD 102807 Induces M3 mAChR-Dependent GRK-/Arrestin-Biased Signaling in Airway Smooth Muscle Cells
- Pharmacological Management of Asthma and COPD
- Specificity of NHERF1 regulation of GPCR signaling and function in human airway smooth muscle
- Regulation of ovarian cancer G protein-coupled receptor-1 expression and signaling
University Appointment
Assistant Professor
Department of Medicine, Division of Pulmonary, Allergy & Critical Care Medicine
Professional Societies
American Thoracic Society
Research & 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.