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01.05.2005

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Each day, your blood travels 19,000 km (12,000 miles) on the circulatory highway. Throughout its journey, a red blood cell (RBC) rides bumper to bumper, enduring dense, merging traffic as it transports its precious load of oxygen or carbon dioxide waste. Like an armored car, the tough blood cell must safeguard the hemoglobin at its center that could damage organs if spilled, yet it must be flexible enough to fold and squeeze into the tiny capillaries where it delivers its load. When RBCs are flawed or malfunctioning, serious, sometimes fatal, illnesses can result.
 
Dr. Nir Gov. Fluctuations mean flexibility
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Dr. Nir Gov of the Chemical Physics Department approaches the puzzle of the red blood cell by studying the physics of its structure, building theoretical models that attempt to explain how this unique cell type’s construction makes it exceptionally well adapted to do its specialized work.
 
Recently, Gov added another, crucial piece to the puzzle. A normal RBC looks like a flattened oval depressed in the center. Helping the cell keep its shape is the cytoskeleton, resembling a springlike wire mesh attached to nodes in the cell's outer membrane. These connections create tension points that hold up the cell wall. It was previously thought that the cell's rigidity/flexibility could be calculated on the basis of the springy properties of the cytoskeleton, but the model developed from this formula wasn’t consistent with experimental results. Something was missing.
 
Working with Prof. Samuel Safran of the Materials and Interfaces Department, Gov found the key to the missing calculation when he took into account the properties of the connections at the nodes. He realized that the presence of ATP, a molecule that converts stored mechanical energy into kinetic motion in the cell, causes transient disassociations and re-associations between the cytoskeleton and the membrane nodes. As tension in the nodes is reduced, motion occurs in the outer membrane. Height fluctuations in the RBC membrane, originally thought to be a negligible effect of small changes in temperature, are instead the result of metabolic activity unique to the living system. This was a defining moment that for Gov highlighted the complexities of modeling dynamic living matter. He proceeded to develop a model linking the presence and concentration of ATP to its effects on cytoskeleton rigidity and, therefore, on RBC shape.
 
RBC models can illuminate important aspects of various diseases and immunities, and these may have vital  impacts on human health research. For example, excessive ATP results in cells that are too flexible, as is the case in some forms of anemia, so that ensuing collisions cause the vulnerable cytoskeleton to break down and the life-giving RBC functionality to be lost. When the ATP level is low, as occurs in some liver diseases, the node connections are too rigid, resulting in stiff, spiky shapes that do not travel smoothly and can block circulation. By modeling, for the first time, ATP’s role in determining the shape and rigidity of the RBC’s outer membrane, Gov has pointed to a completely unexplored avenue of treatment for a number of diseases.
 
In addition, accurate theoretical models might lead the way to creating viable artificial replacements for RBCs. Artificial blood cells could address several problems: rejection, infection and shortages, for example. Gov’s findings might provide a framework for further research in this direction.
 
 
Dr. Nir Gov’s research is supported by the Robert Rees Fund for Applied Research. Dr. Gov is the incumbent of the Alvin and Gertrude Levine Career Development Chair.
 

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