Przemyslaw (Mike) Sapieha, PhD
Canada Research Chair in Retinal Cell Biology
Assistant Professor of Ophthalmology, University of Montreal
Adjunct Professor of Neurology and Neurosurgery McGill University
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
Selected Scientific Contributions
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.
Click here for PubMed listing
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.