Contact info

Dr Przemyslaw (Mike) Sapieha
H�pital Maisonneuve-Rosemont
Centre de Recherche
5415, De l'Assomption boulevard
Montreal, QC H1T 2M4

Tel: 1-514-252-3400, ext. 7711
Fax: 1-514-252-3430
E-mail: [email protected]

Research keywords

Mike Sapieha obtained his BSc in biochemistry from McGill University and in 2005 obtained a PhD in neuroscience and cell biology from the University of Montreal. His graduate work focused on gene therapy for CNS regeneration. He then pursued 2 postdoctoral stages: the first in pharmacology at McGill and the second in ophthalmology at Harvard Medical School. During his postdoctoral training, he worked on the patho-mechanisms of retinopathy of prematurity and the roles of metabolism and lipids in this disease.

In 2010, he joined the departments of ophthalmology and biochemistry at the University of Montreal and opened his research lab at the Maisonneuve-Rosemont Hospital. His research focuses on elucidating the causes of vascular diseases of the retina such as diabetic retinopathy and age-related macular degeneration. In late 2010, he was awarded a Canada Research Chair in Retinal Cell Biology and in 2012 received the first Alcon Young Investigator Award.

Diabetic retinopathy (DR) is the leading cause of blindness in working age adults. It is characterized by microvascular degeneration followed by a disproportionate compensatory hyper-vascularization mounted by the hypoxic retina in an attempt to reinstate metabolic equilibrium. We have identified the classical neuronal repulsive cue Semaphorin 3A in ischemic neural zones of the retina and demonstrated that it is a key vaso-repulsive mediator that prevents reparative angiogenesis in models that serve as proxies for DR (Blood 2011). We have since identified a novel neuronal-immune paradigm whereby mildly ischemic neurons signal to microglia via the classical neuronal guidance Netrin-1 and activate a reparative angiogenesis program (Cell Metabolism, March 2013). In addition, we have recently demonstrated that neuron-derived Semaphorin3A is an early and potent inducer of vascular permeability in diabetic retinopathy (Cell Metabolism, October 2013). Currently, we are developing inhibitors to Semaphorins for ocular applications in partnership with AmorChem.

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The current research focuses in the laboratory fall into three areas:

Neurovascular Cross-Talk in Disease. We seek to identify the mechanisms by which neuronal stress impacts the blood vessels that supply their metabolic needs. We focus on outer retinal neurons and vessels, which are directly affected in diabetes.

Neuroimmune Communication in Disease. Recently, our group has identified a neuroimmune paradigm by which stressed neurons produce non-classical chemoattractive agents that recruit subsets of mononuclear phagocytes to sites of vascular lesion. Further elucidation of these mechanisms is essential to better understanding the pathogenesis of diabetic retinopathy.

Therapeutic Modulation of ω-3-Polyunsaturated fatty acid (PUFA) metabolism for vascular diseases of the retina. Another axis of research in my lab investigates the role of ω-3 PUFAs in angiogenesis and neuronal homeostasis. We have recently described that elevated dietary intake of ω-3 PUFAs lower vitreal VEGF levels in human patients suffering from Age-related Macular Degeneration. Moreover, we identified that certain ω-3 derivatives directly block VEGF-induced pathological angiogenesis.