Page 32 - Rx Bound - Summer 2014
P. 32
Research Spotlight
Investigating the Role of The Transient Receptor Potential
Channel 6 in Platelet Function
Dr. Fadi Khasawneh has been awarded a $140,000 grant by The American Heart
Association for his project, “Investigating the Role of The Transient Receptor
Potential Channel 6 in Platelet Function.”
Thrombosis is a key manifestation of heart attacks and stroke. These two disease states are
major causes of death and suffering in the United States and result in a significant economic
burden on our society. To this end, platelets, one of the blood cells, are key mediators of
thrombosis, and are also known to play an important role in maintaining vascular integrity
based on their ability to respond to lesions in a vessel wall. While hyperactivity of platelets is
known to cause spurious clot formation and occlusive loss of blood flow leading to strokes
and heart attacks, hypoactivity causes bleeding diathesis with life-threatening consequences.
To address and potentially ameliorate the underlying mechanisms of occlusive thrombotic
disease states, it is critical to
understand how platelets respond
Fadi T. Khasawneh, to external stimuli. Based on these
PhD, BPharm considerations, one of the research
goals in our laboratory is to
address fundamental aspects of the
Education biology of one of the calcium
PhD channel proteins, namely the
2007 University of Illinois at transient receptor potential channel
Chicago
6 (abbreviated as TRPC6), that is
known to be found on the surface
BPharm of platelets. Our interest in this
1999 Jordan University of protein derives from the fact that
Science and Technology
while change in intracellular
calcium levels is a central step in
Research Interest platelet activation, its underlying Payam Javaherizadeh, PharmD ’17, Zubair Karim, PhD, Research Assistant
My research is focused on the mechanism is still ill defined, and Professor, Hari Priya Vemana, MSPS Graduate Student, and Fadi T.
study of thrombosis and platelet our belief that TRPCs participate in Khasawneh, PhD, BPharm, Associate Professor of Pharmaceutical Sciences.
biology. Our primary goal is to these processes. Consistent with this notion, our previously published studies had shown that
delineate signaling pathways TRPC6 contributes to the pathogenesis of occlusive thrombotic disorders, such as heart
involved in platelet activation and attacks and stroke, and that it regulates hemostasis (the process of clot formation to prevent
to investigate their role in the blood loss). Thus, the focus of the current work that just received funding from the American
pathogenesis of thrombotic Heart Association (AHA; $140,000 over two years) is to investigate the role of TRPC6 in
diseases. We employ a host of platelet function, and elucidate the underlying mechanism by which it contributes to
molecular, biochemical and thrombogenesis and physiological hemostasis. To achieve our goals, we will employ genetic as
pharmacological approaches, as well as pharmacological approaches.
well as an in vivo Carotid Artery
Thrombosis model in our Collectively, these AHA funded studies address fundamental questions and provide
studies. Our ultimate goal is to mechanistic insight concerning calcium signaling and function downstream of TRPC6 in
identify novel therapeutic targets platelets. Results obtained from these studies should lay down the foundation for defining a
for the management of new therapeutic target, and/or reagents for the therapeutic management of thrombosis-based
thromboembolic disorders. disease states.
30 WesternU, College of Pharmacy
Investigating the Role of The Transient Receptor Potential
Channel 6 in Platelet Function
Dr. Fadi Khasawneh has been awarded a $140,000 grant by The American Heart
Association for his project, “Investigating the Role of The Transient Receptor
Potential Channel 6 in Platelet Function.”
Thrombosis is a key manifestation of heart attacks and stroke. These two disease states are
major causes of death and suffering in the United States and result in a significant economic
burden on our society. To this end, platelets, one of the blood cells, are key mediators of
thrombosis, and are also known to play an important role in maintaining vascular integrity
based on their ability to respond to lesions in a vessel wall. While hyperactivity of platelets is
known to cause spurious clot formation and occlusive loss of blood flow leading to strokes
and heart attacks, hypoactivity causes bleeding diathesis with life-threatening consequences.
To address and potentially ameliorate the underlying mechanisms of occlusive thrombotic
disease states, it is critical to
understand how platelets respond
Fadi T. Khasawneh, to external stimuli. Based on these
PhD, BPharm considerations, one of the research
goals in our laboratory is to
address fundamental aspects of the
Education biology of one of the calcium
PhD channel proteins, namely the
2007 University of Illinois at transient receptor potential channel
Chicago
6 (abbreviated as TRPC6), that is
known to be found on the surface
BPharm of platelets. Our interest in this
1999 Jordan University of protein derives from the fact that
Science and Technology
while change in intracellular
calcium levels is a central step in
Research Interest platelet activation, its underlying Payam Javaherizadeh, PharmD ’17, Zubair Karim, PhD, Research Assistant
My research is focused on the mechanism is still ill defined, and Professor, Hari Priya Vemana, MSPS Graduate Student, and Fadi T.
study of thrombosis and platelet our belief that TRPCs participate in Khasawneh, PhD, BPharm, Associate Professor of Pharmaceutical Sciences.
biology. Our primary goal is to these processes. Consistent with this notion, our previously published studies had shown that
delineate signaling pathways TRPC6 contributes to the pathogenesis of occlusive thrombotic disorders, such as heart
involved in platelet activation and attacks and stroke, and that it regulates hemostasis (the process of clot formation to prevent
to investigate their role in the blood loss). Thus, the focus of the current work that just received funding from the American
pathogenesis of thrombotic Heart Association (AHA; $140,000 over two years) is to investigate the role of TRPC6 in
diseases. We employ a host of platelet function, and elucidate the underlying mechanism by which it contributes to
molecular, biochemical and thrombogenesis and physiological hemostasis. To achieve our goals, we will employ genetic as
pharmacological approaches, as well as pharmacological approaches.
well as an in vivo Carotid Artery
Thrombosis model in our Collectively, these AHA funded studies address fundamental questions and provide
studies. Our ultimate goal is to mechanistic insight concerning calcium signaling and function downstream of TRPC6 in
identify novel therapeutic targets platelets. Results obtained from these studies should lay down the foundation for defining a
for the management of new therapeutic target, and/or reagents for the therapeutic management of thrombosis-based
thromboembolic disorders. disease states.
30 WesternU, College of Pharmacy
