Podor earned his B.Sc. in Biology from the University of Western Ontario
in 1978. He then went on to earn his M.Sc. in Physiology/Biophysics,
and his Ph.D. in Pathology from the University of Southern California
in 1980, and 1984, respectively. During his graduate studies Dr. Podor
studies various aspects of cardiovascular pathophysiology, particularly
the role of endothelial cell proteolytic enzymes in the degradation
of fibrin clots and extracellular matrix components. He then moved to
the Department of Immunology at Scripps Research Institute in La Jolla,
CA where his research involved immunochemical and biochemical studies
on the role of plasminogen activator inhibitor-1 (PAI-1) in thrombosis
and fibrin clot degradation (fibrinolysis). In 1989, he moved back to
Canada and began developed his research program in thrombosis and thrombolysis
at McMaster University.
Dr. Podor's effort to develop new approaches to remove
blood clots through enzymatic and/or mechanical approaches lead him
to consider both the biochemistry and structure of blood clots. His
multidisciplinary research involved (i) studying the effects of inflammatory
mediators on endothelial cell and platelet regulation of fibrinolysis
in various in vitro and in vivo models of thrombosis and vascular injury,
and (ii) defining the specific binding interactions and spatial distribution
of PAI-1, vitronectin, t-PA, and other components in blood clots, damaged
blood vessels, myocardium, and other tissues. His research has lead
him to investigate further the role of PAI-1, vitronectin, t-PA in the
repair and remodeling of hearts damaged by ischemia/infarction, infections,
or transplantation. Thus, to facilitate his studies on damaged hearts,
he moved his laboratory in July 2002 to the McDonald Research Laboratories
(MRL) and iCAPTUR4E Centre at St. Paul's Hospital/ University of British
Columbia. Since arriving, Dr. Podor has also developed a new line of
research involving the use of autologous bone marrow-derived stem cells
to repair and regenerate the damaged myocardium, and to use these stem
cells as a means of introducing cardioprotective transgenes (e.g., t-PA)
into the damaged heart. Much of his work has involved the use of laser
confocal scanning microscopy to visualize the distribution of fluorescently
labeled proteins and cells in tissues. His new laboratory is equipped
with state-of-the-art confocal and two-photon microscopy facilities
suited for advancing three- and four-dimensional imaging technology
for studying cardiovascular disease, and developing animal models for
testing new methods of treating thrombosis, defects in fibrinolysis,
and regenerating damaged myocardium
1. Seiffert D, Geisterfer M,
Gauldie J, Young E and Podor TJ. Interleukin-6
Stimulates Vitronectin Gene Expression In Vivo. J Immunol 155(6):
2. Hill SA, Shaughnessy SG, Joshua P, Ribau J, Austin
RC and Podor TJ. Differential
Mechanisms Targeting Type 1 Plasminogen Activator Inhibitor and Vitronectin
into the Storage Granules of a Human Megakaryocytic Cell Line. Blood
87(12): 5061-5073, 1996.
3. Torry DJ, Richards CD, Podor TJ and Gauldie J.
of the Anchorage-Independent Phenotype of Human Lung Fibroblasts Obtained
from Fibrotic Tissue Following Culture with Retinoid and Corticosteroid.
Exp Lung Res 22(2): 231-244, 1996.
4. Young E, Podor TJ, Venner T and Hirsh J. Induction
of the Acute-Phase Reaction Increases Heparin-Binding Proteins in Plasma.
Arterioscler Thromb Vasc Biol 17(8): 1568-1574, 1997.
5. Wells MJ, Hatton MWC, Hewlett B, Podor TJ, Sheffield
WP and Blajchman MA. Cytokeratin
18 is Expressed on the Hepatocyte Plasma Membrane Surface and Interacts
with Thrombin-Antithrombin Complexes. J Biol Chem 272(45): 28574-28581,
6. Manson L, Weitz JI, Podor TJ, Hirsh J and Young
Variable Anticoagulant Response to Unfractionated Heparin In Vivo Reflects
Binding to Plasma Proteins Rather than Clearance. J Lab Clin Med
130(6): 649-655, 1997.
7. Outinen PA, Sood SK, Liaw PCY, Sarge KD, Maeda
N, Hirsh J, Ribau J, Podor TJ, Weitz JI and Austin RC. Characterization
of the Stress-Inducing Effects of Homocysteine. Biochem J 332(Pt.1):
8. Hayward CPM, Cramer EM, Song Z, Zheng S, Fung R,
Masse J-M, Stead RH and Podor TJ. Studies
of Multimerin in Human Endothelial Cells. Blood 91(4): 1304-1317,
9. Outinen PA, Sood SK, Pfeifer SI, Pamidi S, Podor
TJ, Li J, Weitz, JI and Austin RC. Homocysteine-Induced
Endoplasmic Reticulum Stress and Growth Arrest Leads to Specific Changes
in Gene Expression in Human Vascular Endothelial Cells. Blood 94(3):959-967,
10. Young E, Hirsh J, Shaughnessy S, Ribau J, Venner
T and Podor TJ. The
Binding of Unfractionated Heparin and Low Molecular Weight Heparin to
Thrombin Activated Human Endothelial Cells. Thromb Res 96(5):373-381,
11. Podor TJ, Peterson CB, DA Lawrence, Stefansson,
S, Shaughnessy, SG, Foulon, DM, Butcher, M, and Weitz, JI. Type
1 Plasminogen Activator Inhibitor Binds to Fibrin via Vitronectin.
J Biol Chem 275(26):19788-19794, 2000.
12. Podor, TJ, Shaughnessy, SG, Blackburn, MN, and
Peterson, CB. New
Insights into the Size and Stoichiometry of the Vitronectin: PAI-I Complex..
J Biol Chem 275(33):25402-25410, 2000.
13. Gyorffy, S, Palmer, K, Podor, TJ, Hitt, M, and
Gauldie, J. Combined
Treatment of a Murine Breast cancer Model with the Ad-5 Adenovirus Vectors
Expressing Angiostatin and Interleukin-12: A Role of Combined Anti-Angiogenesis
and Immunotherapy. J. Immunol., 166: 6212-6217, 2001.
14. Kahr, WHA, Zheng, S, Sheth, P, Pai, M, Cowie,
A, Bouchard, M, Podor, TJ, Rivard, GE, and Hayward, CPM. Platelets
from Individuals with the Quebec Platelet Disorder Contain and Secrete
Abnormal Amounts of Urokinase-Type Plasminogen Activator. Blood,
98: 257-265, 2001.
15. Podor, TJ, Campbell, S, Chindemi, P, Farrell,
D, Walton, PR, Weitz, JI, and Peterson, CB. Incorporation
of Vitronectin into Fibrin Clots: Evidence for an Interaction between
Vitronectin and gamma A/gamma' fibrinogen. J Biol Chem, 77(9):7520-7528,
16. Podor, TJ, Singh, D, Foulon, DM, Chindemi,
P, McKelvie, RM, Austin, R, Boudreau, G, and Davies, R.
Vimentin exposed on Activated Platelets and Platelet Microparticles
Localizes Vitronectin and Plasminogen Activator Inhibitor Complexes
on their Surface. J Biol Chem, 77(9): 7529-7539, 2002.