Symposia

VENDREDI 10 OCTOBRE 2025 à partir de 8 h 00 (HNE)

Amphithéâtre A du CRCHUM, 5e étage
900, rue Saint-Denis, Pavillon R, Montréal, Québec, Canada, H2X 0A9

Le Comité organisateur du Symposium est heureux de vous annoncer que le 3e Symposium international sur l’angiogenèse rétinienne et choroïdienne aura lieu le VENDREDI 10 OCTOBRE 2025 à Montréal. Ce symposium est gracieusement soutenu entre autre par le département d’ophtalmologie de l’Université de Montréal, la Fondation Woco et le Réseau de recherche en sciences de la vision. Chercheurs, cliniciens, cliniciens-chercheurs, professionnels de la santé visuelle et étudiants (stagiaires post-doctoraux, deuxième et troisième cycle) sont chaleureusement invités à assister à ce Symposium qui présentera de prestigieuses conférences offertes par des scientifique internationaux et locaux à la fine pointe de la recherche en biologie vasculaire de la rétine.

Programmation scientifique à venir

Les conférenciers

Résumé/Abstract

The Key Role of VEGF in Ocular Andiogenesis

Angiogenesis is a key pathophysiogical process and several families of regulators  have  been implicated at various steps of this process.  Among these regulators, vascular endothelial growth factor (VEGF) and its two tyrosine kinase receptors, VEGFR1 and VEGFR2, represent a key signaling pathway that mediates physiological angiogenesis and are also major therapeutic targets. The importance of VEGF in development is underscored by embryonic lethality in mice after inactivation of only one vegfa allele. VEGF (VEGF-A) is a member of gene family that includes VEGF-B, VEGF-C, VEGF-D and placenta growth factor. In spite of the potential redundancy in the mediators of angiogenesis, all current FDA-approved anti-angiogenic drugs target the VEGF pathway. Indeed, three decades after the initial  isolation and cloning VEGF is arguably one of the most extensively investigated signaling system in angiogenesis. Anti-VEGF agents are widely used in oncology and, in combinations with immunotherapy, are now standard of care in renal or hepatocellular carcinoma. Anti-VEGF therapy have changed the treatment of neovascular eye disorders such as age-related macular degeneration. The benefits of anti-VEGF therapy are durable, provided that patients are followed up regularly and are treated when needed. Much recent data indicate that the availability of VEGF inhibitors has had a dramatic impact on the course of disorders that in the past had no effective treatment. Current research addresses the need to identify additional therapeutic targets for patients that show suboptimal responses to VEGF inhibitors. Efforts are ongoing to determine the translational and clinical significance of such findings.

Résumé/Abstract

Mineralocorticoid pathway activation in retinal pathology

Preclinical and clinical studies have demonstrated beneficial effects of mineralocorticoid receptor antagonists (MRA) in the heart, the vessels and in the kidney at doses that induced only small or no reductions in blood pressure, indicating that inappropriate MR activation exerts direct deleterious effects in various organs and tissues.  In the vessels, the overactivation of the mineralocorticoid receptor (MR), that is expressed in vascular endothelial cells and in smooth muscle cells, is pathogenic through oxidative stress and inflammation, endothelial dysfunction, vascular remodeling, stiffening, and fibrosis, suggesting all organs could be affected if MR pathway is overactivated in the vasculature, at least by indirect vascular effect. In the eye, MR is expressed in the vascular cells of the retina and the choroid, including choriocapillaris and veins and, in cells of neural and glial origins.  MR inappropriate activation, mostly by glucocorticoids contribute to the pathogenesis of diabetic retinopathy, choroidal neovascularization and pachychoroid associated diseases. The potential place of mineralocorticoid receptor antagonists for ocular diseases will be discussed.

Résumé/Abstract

Shaping the vascular tree – principles and regulation of endothelial behaviour

Recent studies identified directional migration behaviour of endothelial cells as a key mechanism in vascular remodelling. Endothelial cells appear to be able to rearrange not only locally, but move considerable distances within perfused vessels. The direction, extent and relative collectiveness of this astonishing behaviour can determine whether individual vessel segments are stabilized or pruned away, change their diameter, and potentially even their fate along the arterio-venous specification spectrum. Failure to properly coordinate and balance directional migration and cell proliferation appears to trigger formation of vascular malformations. Blood flow-dependent apical shear forces are critical for vascular remodelling, and directly impact this directional endothelial migration. Yet, how endothelial cells manage to perform these feats without compromising vascular integrity, what molecular players regulate onset, direction and completion of these processes remains poorly understood. Our recent work on dynamics and regulation of endothelial junctions and in particular junctional actin networks identify new players, and quantitative principles, as well as selective cellular heterogeneity of this behaviour that jointly establish regular vascular patterns. I will provide an update of our current understanding and approaches, and highlight new molecular regulators of this process.

Résumé/Abstract

Hematopoietic stem/progenitor cells mobilize from distinct bone marrow compartments in response to retinal injury

Hematopoietic cells and vascular wall derived endothelial progenitors exist to restore function to damaged endothelium. Much like other tissues,  the bone marrow suffers diabetic end-organ damage, including aberrant adipogenesis, mobilopathy and microangiopathy. Similarly, in diabetics with micro and macrovascular complications, the vascular endothelium is depleted of endothelial progenitor cells (endothelial colony forming cells; ECFC) adversely impacting vessel repair. iPSCs have been generated from many different cells type from both normal and diabetic individuals. iPSCs can be differentiated into hematopoietic cells and ECFCs for vascular repair. We demonstrate the use of a unique hiPSC-derived mesodermal population that promotes robust microvascular repair without any evidence of toxicity. This population was characterized based on expression of VEGFR2, NCAM, and APLNR (KNA+ cells). Both nondiabetic and diabetic donors were used to generate hiPSC lines, and in vitro and in vivo studies were performed to interrogate their function.
The next part of the presentation will discuss specialized bone marrow microenvironments, called niches, inside long and flat bones. The impact of diabetes on the bone marrow niches at different  sites has not been studied. We show that the impact of diabetes is different in the calvaria marrow compartment compared to long bones. The calvarium undergoes slower bone deterioration, reduced  buildup of fat content and less  vascular degeneration compared to the tibia during chronic type 2 diabetes. Cumulatively, this results in a relative preservation of hematopoietic stem and progenitor cell function and an increase in erythroid lineage cells in the calvaria marrow during this period of chronic metabolic insult. Our study suggest that the calvarium is protected from the adverse consequences of diabetes longer than the other bone marrow compartments.

Résumé/Abstract

Targeting pathologic signaling to restore homeostasis in age-related macular degeneration

Age-related macular degeneration (AMD) is a complex common disease that is influenced by genetic predisposition and external stresses, including those associated with aging. Our lab studies signaling effectors triggered by external stresses in choroidal endothelial cells and retinal pigment epithelium (RPE) that lead to features seen in advanced forms of AMD. We identified several important stresses, i.e., angiogenic, inflammatory and oxidative factors, that lead to activation of the GTPase, Rac1, and create feed-ford loops. Binding of active Rac1, Rac1GTP, to a multi-domain protein, IQGAP1, caused Rac1 to remain “on” further driving pathology. We identified another GTPase that interferes with pathologic steps to restore homeostasis of the outer retina.  In addition, we found that oxidized compounds within drusen lead to phenotypic changes in outer retinal cells, and we predict this occurrence may account for some of the cases of poor response to anti-VEGF agents. We study these processes in experimental models.

Résumé/Abstract

Translational Studies in phase I ROP

Retinopathy of prematurity is a two phased disease. Phase I starts after preterm birth as factors that were normally provided by the mother are missing such as omega 3 and omega 6 fatty acids and IGF-1 or are present in excess such as oxygen. As a result, the neural retina and particularly the retinal vasculature fails to mature normally. Starting at about 30 to 32 weeks post menstrual age during the second phase, the slowly developing but avascular neural retina sends signals that are not well regulated for exuberant vascular growth that threatens vision.  At present only the second neovascular phase is treated with photocoagulation to destroy retinal signals for neovascularization or anti-VEGF treatment directed against a major growth factor initiating vascular proliferation. I will discuss studies on prevention by addressing phase I of ROP.

Résumé/Abstract

Laser-assisted technologies enable precise subretinal drug delivery and spatially guided endothelial tubulogenesis

à venir

Résumé/Abstract

Laser-assisted technologies enable precise subretinal drug delivery and spatially guided endothelial tubulogenesis

à venir

Résumé/Abstract

Coronary Angiocrines to Stimulate Heart Regeneration

Alterations in coronary network formation and deficient perfusion of the cardiac muscle lead to myocardial injury and dysfunction.  Efficient revascularization after cardiac damage is essential to support tissue repair and limit scarring.  Contrary to the non-regenerative adult human heart, the zebrafish heart exhibits a remarkable ability to regenerate. The injured zebrafish heart activates a rapid and efficient coronary revascularization response.
We found that regenerating coronaries form a vascular scaffold that supports cardiomyocyte replenishment.  Transcriptomic analyses of coronary endothelial cells allowed us to identify angiocrine factors regulating different aspects of cardiac regeneration.
Our results highlight the importance of coronaries during heart regeneration beyond their role as a transport system and identify pro-regenerative angiocrines.  Simulating these processes in the injured mammalian heart should help its healing.

Résumé/Abstract

Allosteric Modulators of Inflammatory Pathways As Treatments of Retinal and Choroidal Vascular Degeneration

à venir

Résumé/Abstract

Allosteric Modulators of Inflammatory Pathways As Treatments of Retinal and Choroidal Vascular Degeneration

A functional vascular network is a prerequisite for normal embryonic development, tissue repair and engineering. Deciphering the cellular and molecular mechanisms that initiate and regulate blood vessel growth and regression in the retina in homeostatic conditions is key to understand vascular retinopathies. We use unbiased high-throughput screening methods of Single cell RNAseq, combined with microscopy imaging and biochemical analysis to identify angiocrine factors regulating different aspects of vessel remodeling in the eye. We found recently that cellular senescence can occur from the earliest stages of embryonic development and influence endothelial cell’s function. Understanding the cellular and molecular mechanisms of developmental senescence and the identification of new molecular signatures regulating endothelial cell plasticity and specification is of great interest in order to manipulate theses pathways to counteract retinopathy.
Source(s) de financement / Funding : NSERC, CRC-IRSC, VHRN, FCI.
Mots-clés / Keywords : Angiogenesis, endothelial cells, senescence, retina, blood vessels.

Résumé/Abstract

Visualizing Neutrophil Dynamics on the Eye

Microbial keratitis is the inflammation of the cornea, the clear, dome-shaped tissue on the eye, that covers the iris, caused by an infection.  Bacterial keratitis is a common complication in contact lens users, individuals who have suffered eye trauma, and immunocompromised individuals. Both daily and extended wear contact lens users account for up to 66% all bacterial keratitis cases in North America and in Europe. One of the major causative agents of keratitis is the bacteria Pseudomonas aeruginosa. P. aeruginosa is an opportunistic pathogen that is ubiquitously found in the environment. Neutrophils are granulocytic innate immune cells that play a role in both infection control and tissue repair. P. aeruginosa infections are difficult to treat as the bacteria readily form biofilm structures. Bacterial biofilms can tolerate antibiotics and host defenses resulting eye opacity and complete vision loss.  In our work we visualize P. aeruginosa biofilm development and neutrophil recruitment to the infection on the cornea. Neutrophils play a major role in blocking bacterial penetration into the eye and dissemination into the brain but promote biofilm formation in the process of blocking bacterial dissemination. In our work we use a combination of imaging, flow cytometry, and transcriptomics to understand the unique populations of neutrophils in the eye and how they control infection.

CONFÉRENCES DISPONIBLES EN LIGNE: Pour ceux qui sont dans l’impossibilité d’assister en personne à ce symposium, il vous sera possible de suivre les conférences par une diffusion web en direct. Si vous optez pour ce mode de participation, vous recevrez le lien quelques jours avant l’évènement, une fois les frais d’inscription acquittés.

Frais d’inscription et dates limites

Inscriptions hâtives – jusqu’au 31 juillet 2025 (en personne ou en ligne):

Inscriptions – entre le 1er août et le 30 septembre 2025 (en personne ou en ligne):

Formulaire d’inscription disponible bientôt

Le Comité organisateur du Symposium
Sylvain CHEMTOB, M.D. , Ph. D. , FRCPC, FAAP
Isabelle HARDY, M.D., FRCS(C), DABO
Adriana DI POLO, Ph. D.
Bruno LARRIVÉE, Ph. D.
Ian MacDONALD, M.Sc. , M.D., CM
Przemyslaw (Mike) SAPIEHA, Ph. D.
Flavio REZENDE, MD, Ph. D.
Valérie LAVASTRE, Ph. D.
Annie BLAIS, B.A.
Benjamin PELLACANI, B.A.A.

Pour plus d’information, svp contacter Annie Blais (annie.blais.3@umontreal.ca).

Cet évènement n’aurait pas eu lieu sans le support de:

Symposium international sur l’angiogenèse rétinienne et choroïdienne
2e Symposium international  sur l’angiogenèse rétinienne et choroïdienne: de la recherche fondamentale à l’application clinique

Jeudi 20 octobre 2022 à partir de 8 h 00 (HNE)

Pavillon Roger-Gaudry, Université de Montréal – Amphithéâtre M-415
2900 Boul. Edouard-Montpetit, Québec, Canada, H3T 1J4

Le Comité organisateur du Symposium vous remercie d’avoir participé au 2e Symposium international sur l’angiogenèse rétinienne et choroïdienne qui a eu lieu le JEUDI 20 OCTOBRE 2022 à Montréal. Ce symposium fut gracieusement soutenu entre autre par le département d’ophtalmologie de l’Université de Montréal, la Fondation Woco, le Réseau de recherche en santé de la vision et la Fondation Antoine-Turmel.

Chercheurs, cliniciens, cliniciens-chercheurs, professionnels de la santé visuelle et étudiants (stagiaires post-doctoraux, deuxième et troisième cycle) étaient chaleureusement invités à assister à ce Symposium qui présenta de prestigieuses conférences offertes par des scientifique internationaux et locaux à la fine pointe de la recherche en biologie vasculaire de la rétine.

Programmation scientifique

Informations sur les conférenciers

Le Comité organisateur du Symposium
Sylvain CHEMTOB, M.D. , Ph. D. , FRCPC, FAAP
Isabelle HARDY, M.D., FRCS(C), DABO
Adriana DI POLO, Ph. D.
Bruno LARRIVÉE, Ph. D.
Przemyslaw (Mike) SAPIEHA, Ph. D.
Flavio REZENDE, MD, Ph. D.
Valérie LAVASTRE, Ph. D.
Isabelle LAHAIE, M. Sc.
Annie BLAIS, B.A.
Benjamin PELLACANI, B.A.A.

Pour plus d’information, svp contacter Isabelle Lahaie (ilahaie.hmr@ssss.gouv.qc.ca) ou Annie Blais (annie.blais.3@umontreal.ca).

Cet évènement n’aurait pas eu lieu sans le support de:

ACTUALITÉ – COVID-19: Le 2e Symposium international sur l’angiogenèse rétinienne et choroïdienne ne pourra se tenir en présentiel. Soucieux de maintenir une activité scientifique dans ce domaine, le comité organisateur de ce Symposium  vous propose une réunion satellite en mode virtuel.

Réunion scientifique satellite du symposium international sur l’Angiogenese retinienne et choridienne

Jeudi, 5 novembre 2020, 8h30 AM
Heure Normale de l’Est (HNE), UTC-5h

Présentations des conférenciers disponibles

Pour voir ou revoir les conférences, suivez ce lien

La programmation scientifique est maintenant disponible ici: Programme scientifique
Information sur les conférenciers invités: Conférenciers
Cette réunion satellite est organisée conjointement avec l’aide de l’Université de Montréal et du Réseau de recherche de recherche en santé de la vision.
Pour plus d’information, svp contacter Isabelle Lahaie (ilahaie.hmr@ssss.gouv.qc.ca) ou Annie Blais (annie.blais.3@umontreal.ca).

COMITÉ SCIENTIFIQUE ORGANISATEUR
Sylvain CHEMTOB, M.D. , Ph. D. , FRCPC, FAAP
Isabelle HARDY, M.D., FRCS(C), DABO
Adriana DI POLO, Ph. D.
Przemyslaw (Mike) SAPIEHA, Ph. D.
Bruno LARRIVÉE, Ph. D.
Flavio REZENDE, MD, Ph. D.

Résumé/Abstract

Contributions of Neurovascular Abnormalities to Autism Spectrum Disorders

Development of the central nervous system (CNS) relies on proper maturation of its vascular beds that not only ensure steady supply of oxygen and nutrients, but also support the differentiation of neural progenitors. Alterations in vascular processes during CNS development may have long-lasting neurodevelopmental consequences, but direct evidence supporting this concept is missing. Autism spectrum disorders (ASD) are neurodevelopmental conditions that affect attention, memory, learning, motor coordination, language and social interactions. While the neuronal underpinnings of ASD are being extensively studied, whether vascular deficits play a role in ASD onset and/or progression is unknown. To address this important knowledge gap, we investigated the maturation of cerebrovascular networks in 16p11.2df/+ mice, a robust mouse model of the 16p11.2 deletion ASD syndrome. We also achieved endothelial-specific deletion of the 16p11.2 locus by CRE-mediated recombination under the control of an endothelial promoter (16p11.2EC mice). Using both constitutive and conditional mutants, we quantified neurovascular structure and function in vivo and in vitro, and assessed mouse behavior. We demonstrate that 16p11.2 hemizygosity leads to endothelium-dependent structural and functional neurovascular abnormalities.  In 16p11.2df/+ mice, endothelial dysfunction manifested in impaired cerebral angiogenesis at postnatal day (P) 14, and altered neurovascular function at P50.  Defective angiogenesis was also confirmed in vitro using primary 16p11.2df/+ mouse brain endothelial cells, and patient-derived endothelial cells from 16p11.2 deletion carriers. We also found that mice with endothelium-specific 16p11.2 deletion partially recapitulated ASD behavioral traits, including locomotor hyperactivity and altered motor learning. Finally, our more recent work demonstrates a similar brain metabolic shift in both 16p11.2df/+ and 16p11.2EC mice. By revealing that endothelial 16p11.2 homozygosity is required for normal CNS maturation and function, our findings identify endothelial cells as substantial players in ASD.

Résumé/Abstract

Noncanonical TGFb Signaling is Crucial for Specialized Neuroretina Tip-Cells Sprouting and Blood-Retina Barrier Formation

Georgia Zarkada1, Joel P. Howard2, Xue Xiao2,3, Mathilde Bizou2,3, Jinyu Li1, Martin Lange1, Severine Leclerc2, Steffen E. Künzel1, Gael Cagnone2, Jean Sebastien Joyal2, Gregor Andelfinger2, Anne Eichmann1,4#, Alexandre Dubrac2,3,5#1 Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA; 2Centre de Recherche, CHU St. Justine, Montréal, QC, Canada; 3Département de pathologie et biologie cellulaire. Université de Montréal, Montréal, QC, Canada; 4Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA; 5Lead Contact Endothelial sprouting and blood-retina barrier (BRB) are spatiotemporally and carefully orchestrated processes essential for neuroretina homeostasis and proper vision. Mouse retinal vascularization consists of two successive phases. The formation of the superficial vascular plexus is followed by vertical endothelial cell (EC) sprouting, which develops the deep neuroretina vascular layers and establishes the BRB. While these phases both involve VEGF-induced tip cell sprouting, it is not known how the deeper plexus can simultaneously sprout and establish the BRB. Here, using single cell RNA sequencing, we show that diving tip cells (D) constitute a distinct cell population that differs in gene expression and signaling requirements from the superficial tip cells (S). The tip cells D are ESM1– and Mfsd2a+, displaying BRB properties and a TGFb-induced gene signature. Genetic deletion of the TGFb receptor Alk5 in ECs (Alk5iEKO), predominantly affected tip cells D, which became hyperproliferative and hypercontractile, leading to the formation of hemorrhagic glomeruloid tufts and lack of the deep vascular layer. These vascular defects could be rescued by ROCK inhibition, but not cell cycle inhibitors or genetic activation of Wnt signaling. Endothelial deletion of the TGFb downstream SMAD2/3 or SMAD4 effectors did not recapitulate Alk5iEKO phenotypes, suggesting that noncanonical TGFb signaling is essential for neuroretina vascularization. Alk5iEKO mice displayed decreased retinal revascularization during oxygen-induced retinopathy. These data suggest that TGFb signaling could potentially be used therapeutically to promote retinal revascularization and improve neural function in individuals with ischemic retinopathy.

Résumé/Abstract

Brain arteriovenous malformations: genetic origin, signaling and potential therapies

We will review our recent findings of somatic mutations in endothelial cells as a causal event in brain arteriovenous malformation as well as the consequent dysregulation of downstream signaling pathways. We also compare the gene expression in brain AVM endothelial cells with normal adult and developing vasculature at the single cell level. Finally, we will talk about current animal models and potential targeted therapies in brain AVMs.

Résumé/Abstract

Metabolism of the visual cycle and the activity of lecithin retinol acyltransferase from the retinal pigment epithelium

The visual cycle allows to regenerate the visual pigment of photoreceptors after light absorption. The chromophore of the visual pigments is a particular isomer (11-cis) of a derivative of vitamin A, bearing an aldehyde functional group (11-cis retinal, 11cRal). Light absorption leads to the isomerization of this chromophore to all-trans retinal (ATRal). Apo-opsins with no 11cRAL are not responsive to light. 11cRAL must thus be regenerated and recombined with apo-opsins to form light-sensitive visual pigments in photoreceptors. ATRal is thus first converted to all-trans retinol (ATRol) in photoreceptors by retinol dehydrogenase 8. ATRol is subsequently conveyed to the retinal pigment epithelium (RPE) where it will successively be converted to all-trans retinyl ester (ATRes) by the enzyme lecithin retinol acyltransferase (LRAT). The production of ATRes by LRAT needs to be coordinately controlled to sustain normal vision and to protect the retina from photodamage. This involves an uptake of ATRol from blood circulation by the RPE, which is further metabolized by LRAT. ATRes is a lipid-soluble and stable storage form of the visual chromophore in the retinosomes of the RPE. We have characterized the enzymatic activity of a truncated form of LRAT as well as that of mutants of LRAT leading to retinal degeneration. Values of dissociation constants of the ATRol substrate of LRAT have shown almost no difference between native LRAT and its mutants, thus suggesting that this binding is not altered by mutations.

Résumé/Abstract

First Good News of 2020: Gene Therapy in Retinopathies

Dr Rezende will describe the current developments of gene therapy for vitreoretinal diseases.

Le premier symposium International sur l’angiogenèse Rétinienne et Choroïdienne de Montréal a eu lieu le Lundi le 6 novembre 2017 à Montréal. Ce symposium fut organisé dans le cadre de la Réunion annuelle du Réseau de recherche en santé de la vision (RRSV) 2017 et fut soutenu entre autre par l’Université de Montréal, la Fondation Woco et la Fondation Antoine-Turmel.

Près d’une centaine de chercheurs, cliniciens, cliniciens-chercheurs, professionnels de la santé visuelle et d’étudiants (stagiaires post-doctoraux, deuxième et troisième cycle) ont assisté à l’évènement.

Le journal ‘’Annals of Eye Science’’ fut également partenaire de l’évènement.

Une édition spéciale de ce journal (mars 2018) est maintenant accessible en ligne et regroupe les résumés autorisés par les auteurs présentés lors de ce Symposium ainsi que de la Réunion annuelle 2017 du RRSV.

Emplacement où a eu lieu le Symposium: 
Centre de recherche du CHU Ste-Justine
Salle: Amphitéâtre 250 – bloc 11 – niveau A
Adresse: 3175, chemin de la Côte-Sainte-Catherine, Montréal, QC, H3T 1C5

Cet évènement n’aurait pas eu lieu sans le support de: