Eric Shikatani
Cambridge, Massachusetts, United States
584 followers
500+ connections
About
Lab head, Respiratory Diseases. Investigating immunology and fibrosis in respiratory…
Activity
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I’m stunned & honored to receive the 2024 Joseph Loscalzo Award from Circulation for the best basic/translational science paper of the year! Very…
I’m stunned & honored to receive the 2024 Joseph Loscalzo Award from Circulation for the best basic/translational science paper of the year! Very…
Liked by Eric Shikatani
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It has been a great pleasure to develop and run the Intensive CBT Program for Anxiety and OCD at CPG! I am thankful to all of the staff, clinicians…
It has been a great pleasure to develop and run the Intensive CBT Program for Anxiety and OCD at CPG! I am thankful to all of the staff, clinicians…
Liked by Eric Shikatani
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Very pleased to share the first research paper from my lab at Oregon Health & Science University is now out in JCI Insight. Collaborating closely…
Very pleased to share the first research paper from my lab at Oregon Health & Science University is now out in JCI Insight. Collaborating closely…
Liked by Eric Shikatani
Experience
Education
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University of Toronto
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Activities and Societies: • Graduate Curriculum Review Committee, Department of Laboratory Medicine and Pathobiology • Vice-president - Academic, Laboratory Medicine and Pathobiology graduate student association • Academic Advisor, Department of Laboratory Medicine and Pathobiology, University of Toronto • Mentor, Canadian Institutes of Health Research Synapse program • Trainee Member, American Heart Association • Trainee Member, Hypertension Canada • Cardiovascular Sciences Collaborative Program, University of Toronto
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Activities and Societies: York University Kendo Club, Varsity Rugby
Publications
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S-Nitrosoglutathione Reductase Deficiency Confers Improved Survival and Neurological Outcome in Experimental Cerebral Malaria
Infection and Immunity
Artesunate remains the mainstay of treatment for cerebral malaria, but it is less effective in later stages of disease when the host inflammatory response and blood-brain barrier integrity dictate clinical outcomes. Nitric oxide (NO) is an important regulator of inflammation and microvascular integrity, and impaired NO bioactivity is associated with fatal outcomes in malaria. Endogenous NO bioactivity in mammals is largely mediated by S-nitrosothiols (SNOs). Based on these observations, we…
Artesunate remains the mainstay of treatment for cerebral malaria, but it is less effective in later stages of disease when the host inflammatory response and blood-brain barrier integrity dictate clinical outcomes. Nitric oxide (NO) is an important regulator of inflammation and microvascular integrity, and impaired NO bioactivity is associated with fatal outcomes in malaria. Endogenous NO bioactivity in mammals is largely mediated by S-nitrosothiols (SNOs). Based on these observations, we hypothesized that animals deficient in the SNO-metabolizing enzyme, S-nitrosoglutathione reductase (GSNOR), which exhibit enhanced S-nitrosylation, would have improved outcomes in a preclinical model of cerebral malaria. GSNOR knockout (KO) mice infected with Plasmodium berghei ANKA had significantly delayed mortality compared to WT animals (P < 0.0001), despite higher parasite burdens (P < 0.01), and displayed markedly enhanced survival versus the wild type (WT) when treated with the antimalarial drug artesunate (77% versus 38%; P < 0.001). Improved survival was associated with higher levels of protein-bound NO, decreased levels of CD4+ and CD8+ T cells in the brain, improved blood-brain barrier integrity, and improved coma scores, as well as higher levels of gamma interferon. GSNOR KO animals receiving WT bone marrow had significantly reduced survival following P. berghei ANKA infection compared to those receiving KO bone barrow (P < 0.001). Reciprocal transplants established that survival benefits of GSNOR deletion were attributable primarily to the T cell compartment. These data indicate a role for GSNOR in the host response to malaria infection and suggest that strategies to disrupt its activity will improve clinical outcomes by enhancing microvascular integrity and modulating T cell tissue tropism.
Other authorsSee publication -
Paradoxical Suppression of Atherosclerosis in the Absence of microRNA-146a
Circulation Research
RATIONALE:
Inflammation is a key contributor to atherosclerosis. MicroRNA-146a (miR-146a) has been identified as a critical brake on proinflammatory nuclear factor κ light chain enhancer of activated B cells signaling in several cell types, including endothelial cells and bone marrow (BM)-derived cells. Importantly, miR-146a expression is elevated in human atherosclerotic plaques, and polymorphisms in the miR-146a precursor have been associated with risk of coronary artery…RATIONALE:
Inflammation is a key contributor to atherosclerosis. MicroRNA-146a (miR-146a) has been identified as a critical brake on proinflammatory nuclear factor κ light chain enhancer of activated B cells signaling in several cell types, including endothelial cells and bone marrow (BM)-derived cells. Importantly, miR-146a expression is elevated in human atherosclerotic plaques, and polymorphisms in the miR-146a precursor have been associated with risk of coronary artery disease.
METHODS AND RESULTS:
Paradoxically, Ldlr-/- (low-density lipoprotein receptor null) mice deficient in miR-146a develop less atherosclerosis, despite having highly elevated levels of circulating proinflammatory cytokines. In contrast, cytokine levels are normalized in Ldlr-/-;miR-146a-/- mice receiving wild-type BM transplantation, and these mice have enhanced endothelial cell activation and elevated atherosclerotic plaque burden compared with Ldlr-/- mice receiving wild-type BM, demonstrating the atheroprotective role of miR-146a in the endothelium. We find that deficiency of miR-146a in BM-derived cells precipitates defects in hematopoietic stem cell function, contributing to extramedullary hematopoiesis, splenomegaly, BM failure, and decreased levels of circulating proatherogenic cells in mice fed an atherogenic diet. These hematopoietic phenotypes seem to be driven by unrestrained inflammatory signaling that leads to the expansion and eventual exhaustion of hematopoietic cells, and this occurs in the face of lower levels of circulating low-density lipoprotein cholesterol in mice lacking miR-146a in BM-derived cells. Furthermore, we identify sortilin-1(Sort1), a known regulator of circulating low-density lipoprotein levels in humans, as a novel target of miR-146a.
CONCLUSIONS:
Our study reveals that miR-146a regulates cholesterol metabolism and tempers chronic inflammatory responses to atherogenic diet by restraining proinflammatory signaling in endothelial cells and BM-derived cells.Other authorsSee publication -
c-Myb regulates proliferation and differentiation of adventitial Sca1+ vascular smooth muscle cell progenitors by transactivation of myocardin
Atherosclerosis, Thrombosis, and Vascular Biology
Vascular smooth muscle cells (VSMCs) are believed to dedifferentiate and proliferate in response to vessel injury. Recently, adventitial progenitor cells were implicated as a source of VSMCs involved in vessel remodeling. c-Myb is a transcription factor known to regulate VSMC proliferation in vivo and differentiation of VSMCs from mouse embryonic stem cell–derived progenitors in vitro. However, the role of c-Myb in regulating specific adult vascular progenitor cell populations was not known…
Vascular smooth muscle cells (VSMCs) are believed to dedifferentiate and proliferate in response to vessel injury. Recently, adventitial progenitor cells were implicated as a source of VSMCs involved in vessel remodeling. c-Myb is a transcription factor known to regulate VSMC proliferation in vivo and differentiation of VSMCs from mouse embryonic stem cell–derived progenitors in vitro. However, the role of c-Myb in regulating specific adult vascular progenitor cell populations was not known. Our objective was to examine the role of c-Myb in the proliferation and differentiation of Sca1+ adventitial VSMC progenitor cells.
Other authorsSee publication -
Glucagon-Like Peptide 1 Receptor Activation Attenuates Platelet Aggregation and Thrombosis
Diabetes
Short-term studies in subjects with diabetes receiving glucagon-like peptide 1 (GLP-1)–targeted therapies have suggested a reduced number of cardiovascular events. The mechanisms underlying this unexpectedly rapid effect are not known. We cloned full-length GLP-1 receptor (GLP-1R) mRNA from a human megakaryocyte cell line (MEG-01), and found expression levels of GLP-1Rs in MEG-01 cells to be higher than those in the human lung but lower than in the human pancreas. Incubation with GLP-1 and the…
Short-term studies in subjects with diabetes receiving glucagon-like peptide 1 (GLP-1)–targeted therapies have suggested a reduced number of cardiovascular events. The mechanisms underlying this unexpectedly rapid effect are not known. We cloned full-length GLP-1 receptor (GLP-1R) mRNA from a human megakaryocyte cell line (MEG-01), and found expression levels of GLP-1Rs in MEG-01 cells to be higher than those in the human lung but lower than in the human pancreas. Incubation with GLP-1 and the GLP-1R agonist exenatide elicited a cAMP response in MEG-01 cells, and exenatide significantly inhibited thrombin-, ADP-, and collagen-induced platelet aggregation. Incubation with exenatide also inhibited thrombus formation under flow conditions in ex vivo perfusion chambers using human and mouse whole blood. In a mouse cremaster artery laser injury model, a single intravenous injection of exenatide inhibited thrombus formation in normoglycemic and hyperglycemic mice in vivo. Thrombus formation was greater in mice transplanted with bone marrow lacking a functional GLP-1R (Glp1r−/−), compared with those receiving wild-type bone marrow. Although antithrombotic effects of exenatide were partly lost in mice transplanted with bone marrow from Glp1r−/− mice, they were undetectable in mice with a genetic deficiency of endothelial nitric oxide synthase. The inhibition of platelet function and the prevention of thrombus formation by GLP-1R agonists represent potential mechanisms for reduced atherothrombotic events.
Other authorsSee publication -
Self-renewing resident arterial macrophages arise from embryonic CX3CR1+ precursors and circulating monocytes immediately after birth
Nature Immunology
Resident macrophages densely populate the normal arterial wall, yet their origins and the mechanisms that sustain them are poorly understood. Here we use gene-expression profiling to show that arterial macrophages constitute a distinct population among macrophages. Using multiple fate-mapping approaches, we show that arterial macrophages arise embryonically from CX3CR1+ precursors and postnatally from bone marrow–derived monocytes that colonize the tissue immediately after birth. In adulthood…
Resident macrophages densely populate the normal arterial wall, yet their origins and the mechanisms that sustain them are poorly understood. Here we use gene-expression profiling to show that arterial macrophages constitute a distinct population among macrophages. Using multiple fate-mapping approaches, we show that arterial macrophages arise embryonically from CX3CR1+ precursors and postnatally from bone marrow–derived monocytes that colonize the tissue immediately after birth. In adulthood, proliferation (rather than monocyte recruitment) sustains arterial macrophages in the steady state and after severe depletion following sepsis. After infection, arterial macrophages return rapidly to functional homeostasis. Finally, survival of resident arterial macrophages depends on a CX3CR1-CX3CL1 axis within the vascular niche.
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Thioredoxin-Interacting Protein Deficiency Protects against Diabetic Nephropathy
Journal of the American Society of Nephrology
Expression of thioredoxin-interacting protein (TxNIP), an endogenous inhibitor of the thiol oxidoreductase thioredoxin, is augmented by high glucose (HG) and promotes oxidative stress. We previously reported that TxNIP-deficient mesangial cells showed protection from HG-induced reactive oxygen species, mitogen-activated protein kinase phosphorylation, and collagen expression. Here, we investigated the potential role of TxNIP in the pathogenesis of diabetic nephropathy (DN) in vivo. Wild-type…
Expression of thioredoxin-interacting protein (TxNIP), an endogenous inhibitor of the thiol oxidoreductase thioredoxin, is augmented by high glucose (HG) and promotes oxidative stress. We previously reported that TxNIP-deficient mesangial cells showed protection from HG-induced reactive oxygen species, mitogen-activated protein kinase phosphorylation, and collagen expression. Here, we investigated the potential role of TxNIP in the pathogenesis of diabetic nephropathy (DN) in vivo. Wild-type (WT) control, TxNIP−/−, and TxNIP+/− mice were rendered equally diabetic with low-dose streptozotocin. In contrast to effects in WT mice, diabetes did not increase albuminuria, proteinuria, serum cystatin C, or serum creatinine levels in TxNIP−/− mice. Whereas morphometric studies of kidneys revealed a thickened glomerular basement membrane and effaced podocytes in the diabetic WT mice, these changes were absent in the diabetic TxNIP−/− mice. Immunohistochemical analysis revealed significant increases in the levels of glomerular TGF-β1, collagen IV, and fibrosis only in WT diabetic mice. Additionally, only WT diabetic mice showed significant increases in oxidative stress (nitrotyrosine, urinary 8-hydroxy-2-deoxy-guanosine) and inflammation (IL-1β mRNA, F4/80 immunohistochemistry). Expression levels of Nox4-encoded mRNA and protein increased only in the diabetic WT animals. A significant loss of podocytes, assessed by Wilms’ tumor 1 and nephrin staining and urinary nephrin concentration, was found in diabetic WT but not TxNIP−/− mice. Furthermore, in cultured human podocytes exposed to HG, TxNIP knockdown with siRNA abolished the increased mitochondrial O2− generation and apoptosis. These data indicate that TxNIP has a critical role in the progression of DN and may be a promising therapeutic target.
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Inhibition of Src Kinase Blocks High Glucose–Induced EGFR Transactivation and Collagen Synthesis in Mesangial Cells and Prevents Diabetic Nephropathy in Mice
Diabetes
Chronic exposure to high glucose leads to diabetic nephropathy characterized by increased mesangial matrix protein (e.g., collagen) accumulation. Altered cell signaling and gene expression accompanied by oxidative stress have been documented. The contribution of the tyrosine kinase, c-Src (Src), which is sensitive to oxidative stress, was examined. Cultured rat mesangial cells were exposed to high glucose (25 mmol/L) in the presence and absence of Src inhibitors (PP2, SU6656), Src small…
Chronic exposure to high glucose leads to diabetic nephropathy characterized by increased mesangial matrix protein (e.g., collagen) accumulation. Altered cell signaling and gene expression accompanied by oxidative stress have been documented. The contribution of the tyrosine kinase, c-Src (Src), which is sensitive to oxidative stress, was examined. Cultured rat mesangial cells were exposed to high glucose (25 mmol/L) in the presence and absence of Src inhibitors (PP2, SU6656), Src small interfering RNA (siRNA), and the tumor necrosis factor-α–converting enzyme (TACE) inhibitor, TAPI-2. Src was investigated in vivo by administration of PP2 to streptozotocin (STZ)-induced diabetic DBA2/J mice. High glucose stimulated Src, TACE, epidermal growth factor receptor (EGFR), mitogen-activated protein kinases (MAPKs), extracellular signal–regulated kinase (ERK1/2, p38), and collagen IV accumulation in mesangial cells. PP2 and SU6656 blocked high glucose–stimulated phosphorylation of Src Tyr-416, EGFR, and MAPKs. These inhibitors and Src knockdown by siRNA, as well as TAPI-2, also abrogated high glucose–induced phosphorylation of these targets and collagen IV accumulation. In STZ-diabetic mice, albuminuria, increased Src pTyr-416, TACE activation, ERK and EGFR phosphorylation, glomerular collagen accumulation, and podocyte loss were inhibited by PP2. These data indicate a role for Src in a high glucose-Src-TACE-heparin-binding epidermal growth factor-EGFR-MAPK–signaling pathway to collagen accumulation. Thus, Src may provide a novel therapeutic target for diabetic nephropathy.
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Local proliferation dominates lesional macrophage accumulation in atherosclerosis
Nature Medicine
During the inflammatory response that drives atherogenesis, macrophages accumulate progressively in the expanding arterial wall. The observation that circulating monocytes give rise to lesional macrophages has reinforced the concept that monocyte infiltration dictates macrophage buildup. Recent work has indicated, however, that macrophage accumulation does not depend on monocyte recruitment in some inflammatory contexts. We therefore revisited the mechanism underlying macrophage accumulation in…
During the inflammatory response that drives atherogenesis, macrophages accumulate progressively in the expanding arterial wall. The observation that circulating monocytes give rise to lesional macrophages has reinforced the concept that monocyte infiltration dictates macrophage buildup. Recent work has indicated, however, that macrophage accumulation does not depend on monocyte recruitment in some inflammatory contexts. We therefore revisited the mechanism underlying macrophage accumulation in atherosclerosis. In murine atherosclerotic lesions, we found that macrophages turn over rapidly, after 4 weeks. Replenishment of macrophages in these experimental atheromata depends predominantly on local macrophage proliferation rather than monocyte influx. The microenvironment orchestrates macrophage proliferation through the involvement of scavenger receptor A (SR-A). Our study reveals macrophage proliferation as a key event in atherosclerosis and identifies macrophage self-renewal as a therapeutic target for cardiovascular disease.
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A Glucagon-Like Peptide-1 Analog Reverses the Molecular Pathology and Cardiac Dysfunction of a Mouse Model of Obesity
Circulation
Cardiac consequences of obesity include inflammation, hypertrophy, and compromised energy metabolism. Glucagon-like peptide-1 is an incretin hormone capable of cytoprotective actions that reduces inflammation and endoplasmic reticulum stress in other tissues. Here we examine the cardiac effects of the glucagon-like peptide-1 analog liraglutide in a model of obesity, independent of changes in body weight.
C57Bl6 mice were placed on a 45% high-fat diet (HFD) or a regular chow diet. Mice on…Cardiac consequences of obesity include inflammation, hypertrophy, and compromised energy metabolism. Glucagon-like peptide-1 is an incretin hormone capable of cytoprotective actions that reduces inflammation and endoplasmic reticulum stress in other tissues. Here we examine the cardiac effects of the glucagon-like peptide-1 analog liraglutide in a model of obesity, independent of changes in body weight.
C57Bl6 mice were placed on a 45% high-fat diet (HFD) or a regular chow diet. Mice on HFD developed 46±2% and 60±2% greater body weight relative to regular chow diet–fed mice at 16 and 32 weeks, respectively (both P<0.0001), manifesting impaired glucose tolerance, insulin resistance, and cardiac ceramide accumulation by 16 weeks. One-week treatment with liraglutide (30 µg/kg twice daily) did not reduce body weight, but reversed insulin resistance, cardiac tumor necrosis factor-α expression, nuclear factor kappa B translocation, obesity-induced perturbations in cardiac endothelial nitric oxide synthase, connexin-43, and markers of hypertrophy and fibrosis, in comparison with placebo-treated HFD controls. Liraglutide improved the cardiac endoplasmic reticulum stress response and also improved cardiac function in animals on HFD by an AMP-activated protein kinase–dependent mechanism. Supporting a direct mechanism of action, liraglutide (100 nmol/L) prevented palmitate-induced lipotoxicity in isolated mouse cardiomyocytes and primary human coronary smooth muscle cells and prevented adhesion of human monocytes to tumor necrosis factor-α–activated human endothelial cells in vitro.
Weight-neutral treatment with a glucagon-like peptide-1 analog activates several cardioprotective pathways, prevents HFD-induced insulin resistance and inflammation, reduces monocyte vascular adhesion, and improves cardiac function in vivo by activating AMP-activated protein kinase. These data support a role for glucagon-like peptide-1 analogs in limiting the cardiovascular risks of obesity.
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Serum-free differentiation of functional human coronary-like vascular smooth muscle cells from embryonic stem cells
Cardiovascular Research
Aims Despite the diverse developmental origins of vascular smooth muscle cells (VSMCs), recent attempts to generate VSMCs from human embryonic stem cells (hESCs) differentiated along various lineages did not yield distinct cell phenotypes. The aim of this study was to derive and characterize functional coronary-like VSMCs from hESCs using serum-free cardiac-directed differentiation.
Methods and results Embryoid bodies (EBs) from three pluripotent stem cell lines subjected to…
Aims Despite the diverse developmental origins of vascular smooth muscle cells (VSMCs), recent attempts to generate VSMCs from human embryonic stem cells (hESCs) differentiated along various lineages did not yield distinct cell phenotypes. The aim of this study was to derive and characterize functional coronary-like VSMCs from hESCs using serum-free cardiac-directed differentiation.
Methods and results Embryoid bodies (EBs) from three pluripotent stem cell lines subjected to cardiac-directed differentiation in defined media were characterized over 30 days for VSMC-specific gene expression by qRT–PCR, immunofluorescence microscopy and fluorescence-activated cell sorting (FACS). EBs composed of cardiomyocytes, endothelial cells (ECs), fibroblasts, and VSMCs underwent FACS on d28 to reveal that the VSMCs form a distinct subpopulation, which migrate with ECs in an in vitro angiogenesis assay. To enrich for VSMCs, d28 EBs were dissociated and cultured as monolayers. Over several passages, mRNA and protein levels of cardiomyocyte, endothelial, and fibroblast markers were abolished, whereas those of mature VSMCs were unchanged. Vascular endothelial growth factor and basic fibroblast growth factor were critical for the separation of the cardiac and VSMC lineages in EBs, and for the enrichment of functional VSMCs in monolayer cultures. Calcium cycling and cell shortening responses to vasoconstrictors in hESC-derived VSMCs in vitro were indistinguishable from primary human coronary artery SMCs, and distinct from bladder and aorta SMCs. VSMCs identically derived from green fluorescent protein -expressing hESCs integrated in and contributed to new vessel formation in vivo.
Conclusion The ability to generate hESC-derived functional human coronary-like VSMCs in serum-free conditions has implications for disease modelling, drug screening, and regenerative therapies.
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Inhibition of Proliferation, Migration and Proteolysis Contribute to Corticosterone-Mediated Inhibition of Angiogenesis
PLOS One
The angiostatic nature of pharmacological doses of glucocorticoid steroids is well known. However, the consequences of pathophysiological elevation of endogenous glucocorticoids are not well established. In the current study, we hypothesized that the angiostatic effect of corticosterone, an endogenous glucocorticoid in rodents, occurs through multi-faceted alterations in skeletal muscle microvascular endothelial cell proliferation, migration, and proteolysis. Chronic corticosterone treatment…
The angiostatic nature of pharmacological doses of glucocorticoid steroids is well known. However, the consequences of pathophysiological elevation of endogenous glucocorticoids are not well established. In the current study, we hypothesized that the angiostatic effect of corticosterone, an endogenous glucocorticoid in rodents, occurs through multi-faceted alterations in skeletal muscle microvascular endothelial cell proliferation, migration, and proteolysis. Chronic corticosterone treatment significantly reduced the capillary to fiber ratio in the tibialis anterior muscle compared to that of placebo-treated rats. Corticosterone inhibited endothelial cell sprouting from capillary segments ex vivo. Similarly, 3-dimensional endothelial cell spheroids treated with corticosterone for 48 hours showed evidence of sprout regression and reduced sprout length. Endothelial cell proliferation was reduced in corticosterone treated cells, coinciding with elevated FoxO1 and reduced VEGF production. Corticosterone treated endothelial cells exhibited reduced migration, which correlated with a reduction in RhoA activity. Furthermore, corticosterone treated endothelial cells in both 3-dimensional and monolayer cultures had decreased MMP-2 production and activation resulting in decreased proteolysis by endothelial cells, limiting their angiogenic potential. Promoter assays revealed that corticosterone treatment transcriptionally repressed MMP-2, which may map to a predicted GRE between −1510 and −1386 bp of the MMP-2 promoter. Additionally, Sp1, a known transcriptional activator of MMP-2 was decreased following corticosterone treatment. This study provides new insights into the mechanisms by which pathophysiological levels of endogenous glucocorticoids may exert angiostatic effects.
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Honors & Awards
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1st place, Poster competition, Michael J. Sole Annual Cardiovascular Scientific Day
Heart & Stroke/Richard Lewar Centre of Excellence
• Awarded $1,000
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School of Graduate Studies Conference Grant
University of Toronto
• Awarded $1,570
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2nd place, Manuscript competition, Mimi and Charles Hollenberg Research Competition
University Health Network/Mount Sinai Hospital
• Awarded $500
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Canadian Hypertension Congress Travel Award
Hypertension Canada
• Awarded $600
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1st place, Poster competition, 16th Annual Graduate Student Research Day
Department of Laboratory Medicine and Pathobiology, University of Toronto
• Awarded $150
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1st place, Poster competition, Toronto General Research Institute Research Day
Toronto General Research Institute
• Awarded $125
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ATVB Travel Award for Young Investigators
American Heart Association
• Awarded $500
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Canadian Hypertension Congress Travel Award
Hypertension Canada
• Awarded $650
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Council on Basic Cardiovascular Science Travel Award
European Society for Cardiology
• Awarded €500
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2nd Place, Poster competition, 15th Annual Graduate Student Research Day
Department of Laboratory Medicine and Pathobiology, University of Toronto
• Awarded $50
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Best Presentation, 13th Annual Student Research Day
Cardiovascular Sciences Collaborative Program, University of Toronto
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Canadian Hypertension Congress Travel Award
Hypertension Canada
• Awarded $150
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Doctoral Research Award, Priority Area: Hypertension
Canadian Institutes of Health Research
• Awarded $105,000 ($35,000/year for 3 years)
• Canadian Institutes of Health Research (Canadian NIH-equivalent) scholarship awarded for demonstrated research excellence and future research potential.
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Travel Award – Young Investigator’s Forum
CIHR Institute of Circulatory and Respiratory Health
• Awarded $758
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Canadian Hypertension Congress Travel Award
Hypertension Canada
• Awarded $450
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Meredith & Malcolm Silver Scholarship in Cardiovascular Studies
Department of Laboratory Medicine and Pathobiology, University of Toronto
• Awarded $2,075
• Awarded for maintaining honour standing with a demonstrated interest in cardiovascular research.
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Ontario Graduate Scholarship
University of Toronto
• Awarded $15,000
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University of Toronto Graduate Fellowship
University of Toronto
• Awarded $5,000
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Student Annual Meeting Award
American Association of Anatomists
• Awarded $250
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Conference travel award
CIHR Institute of Circulatory and Respiratory Health
• Awarded $1,300
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Heart and Stroke Foundation Master’s Studentship Award
Heart and Stroke Foundation of Ontario
• Awarded $36,000 ($18,500/year for two years)
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Dr. James Wu Research Internship
Faculty of Science and Engineering, York University. (Undergraduate research award)
• Awarded $7,500
• Undergraduate research award; one of three awardees across entire Faculty of Science. Renewed for summer term ($5,000).
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Scholarships and Awards: 23 | $179,253 total
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Languages
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English
Native or bilingual proficiency
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Japanese
Native or bilingual proficiency
More activity by Eric
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Please join us tomorrow! 😁 #career #pharmaindustry #careerdevelopment #careeradvice #lablife #postdoc #careerjourney
Please join us tomorrow! 😁 #career #pharmaindustry #careerdevelopment #careeradvice #lablife #postdoc #careerjourney
Liked by Eric Shikatani
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Are you a translational immunologist interested in a role that spans pre-clinical to late clinical phases focused on identifying and developing…
Are you a translational immunologist interested in a role that spans pre-clinical to late clinical phases focused on identifying and developing…
Liked by Eric Shikatani
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When we started our journey a little over three years ago, we set out to pioneer a new era of precision oncology by integrating the latest…
When we started our journey a little over three years ago, we set out to pioneer a new era of precision oncology by integrating the latest…
Liked by Eric Shikatani
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I’m happy to share that I’m starting a new position as Director, Oncology Search and Evaluation at Merck!
I’m happy to share that I’m starting a new position as Director, Oncology Search and Evaluation at Merck!
Liked by Eric Shikatani
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That’s a wrap! It’s been 10 years, 4 months and 13 days since I stepped foot on the Horsham site in the UK to start what has been the most memorable…
That’s a wrap! It’s been 10 years, 4 months and 13 days since I stepped foot on the Horsham site in the UK to start what has been the most memorable…
Liked by Eric Shikatani
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“Some people have a misunderstanding that a drug comes from high-throughput screening – that we screen millions of compounds and at the end of that…
“Some people have a misunderstanding that a drug comes from high-throughput screening – that we screen millions of compounds and at the end of that…
Liked by Eric Shikatani
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