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À tous les professeurs, étudiants et partenaires du Département de pharmacologie et physiologie,
Vous êtes cordialement invités aux conférences scientifiques du Département de pharmacologie et physiologie qui ont lieu les jeudis, de 9 h à 10 h.
Vous pouvez consulter l’horaire à l’adresse suivante :
https://pharmacologie-physiologie.umontreal.ca/departement/conferences/.
Prochaine conférence : Jeudi 27 octobre 2022 à 9 h
Conférencier : Terry Hebert, PhD.
Professor, Department of Pharmacology and Therapeutics, School of Biomedical Sciences / Director, McGill Regenerative Medicine Network Faculty of Medicine and Health Sciences, McGill University
Combining biosensors and iPSCs to understand GPCR function in cardiomyocytes
To truly personalize medicine, we must be able to model disease on a patient-specific basis. We have enrolled patients diagnosed with dilated cardiomyopathy (DCM) of diverse etiologies as well as numerous control subjects. They are at various stages of disease progression and currently take a wide array of standard heart failure medications. Using peripheral blood mononuclear cells (PBMCs), we generate induced pluripotent stem cell (iPSC) lines and deriving cardiovascular-relevant cells from them. Surprisingly, the same small group of signalling receptors control normal, adaptive, and maladaptive responses to neurohormonal stimulation in the heart. However, what controls decisions regarding physiological versus pathophysiological signalling events remains unknown. Experimental evidence suggests that cellular signalling networks or signalling “hubs” that control cell function and fate are cell- and tissue-type specific. Each signalling “hub” is also influenced by a patient’s personalized genetic profile. Spatiotemporal aspects of signalling are thus determined by how these signalling hubs are altered in disease. Considering that DCM is largely characterized as ventricular dilation with systolic dysfunction, we anticipate that the underlying pathophysiological mechanisms leading to this state are not unique in each patient but recur in several patients. We believe that the systematic mapping of signalling outcomes in healthy versus DCM patient-derived iPSC-CMs will help identify of a core number of deregulated pathways and will facilitate our understanding of the influence of cell context on disease evolution. We have engineered patient and control iPSC lines and have derived cardiomyocytes from all of them. Our iPSC-based platforms give us the means to study these events in multiple cell types relevant to the cardiovascular system in health and disease right down to the single cell level using resonance energy transfer-based biosensors. Our working hypothesis is that the molecular underpinnings of dilated cardiomyopathy can be clustered into a finite number of phenotypic and signalling subtypes. Our strategy is to leverage patient-derived cardiomyocytes to understand how to approach survival and function of these cells in response to currently used therapies.
Endroit : Pavillon Roger-Gaudry, local N425-3
Responsable : Rafael Najmanovich
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