JULIA M. ROSS
Assistant Professor
B.S., Chemical Engineering, Purdue University, 1990.
Ph.D., Chemical Engineering, Rice University, 1994.
My research interests involve the application of chemical engineering principles to solve questions concerning the molecular mechanisms of cell adhesion under dynamic conditions. Video microscopy coupled with digital image processing allows direct visual observation and quantitation of cellular adhesion and aggregation events in real-time. Parallel plate flow chambers are employed to create well defined conditions of wall shear rate and shear stress. In addition, flow cytometry can be used to measure several cell parameters at once, including size, granularity, morphology and specific molecular receptor expression using fluorescence markers (such as labeled monoclonal antibodies). These measuring capabilities allow differentiation of cell types in heterogeneous samples and the quick and easy determination of the presence of cell surface receptors. The ultimate goal is to identify and understand the molecular mechanisms involved in cell adhesion in order to manipulate either cells or surfaces to increase or prevent adhesion as desired.
Molecular Mechanisms of Microbial Adhesion. Biomedical Applications. Bacterial adherence to host tissues is the crucial first step in the development of many bacterial infections. The adhesion of bacteria is predominantly dependent on specific interactions between cell surface receptors and ligands in the host tissue. Both gram-negative and gram-positive bacteria, as well as yeast cells, have been shown to bind extracellular matrix proteins with a high degree of specificity and affinity. These interactions have been proposed to mediate microbial adherence to host tissues where the tissue location of the matrix protein may impose tissue specificity of the infection. The adhesion of various microbes to matrix proteins has been well studied under static conditions. However, in many cases, these interactions occur physiologically under dynamic shear conditions. Consequently, the molecular surface characteristics of the bacteria and biomaterial (or subendothelium) will govern the probability of an adhesive interaction, while the local hemodynamics will determine the kinetics of the process.
Molecular Mechanisms of Platelet Adhesion. Blood platelets play a crucial role in both hemostatis and thrombosis. Intact blood vessels are lined with endothelial cells, which under normal conditions prevent the interaction of platelets with the subendothelium. Upon injury to a blood vessel, endothelial cells lining the vessel are damaged thereby exposing the extracellular matrix to platelets. Platelets then adhere via specific membrane receptors to a variety of macromolecules in the subendothelium. This is the initial event in a cascade that leads to the formation of platelets aggregates to plug the site of injury and prevent the blood loss. A complex biochemical reaction cascade accompanies this process and culminates in clot formation. Due to this ability, platelets also have a central role in thrombosis, or the formation of intravascular clots that impede the flow of the blood. The pathalogical process of thrombosis is implicated in myocardial infarction and stroke. Therapies to cure thrombosis must balance between interfering with platelet adhesion and subsequent aggregation in the thrombotic case, and retaining hemostatic capability. Because the vasculature is a dynamic system, knowledge of local fluid dynamics involved in the flow of blood at a wound site is crucial to understanding the kinetics of platelet adhesion and aggregation. For a platelet to become attached to blood vessel wall, it must withstand the drag force of blood moving adjacent to the vessel wall. In addition, the fluid shear stresses in the circulation act on the surface of the platelets where they may alter the structure, clustering, or exposure of molecules in the cell membrane thus potentially altering cellular responses to biochemical stimuli. Therefore it known that mechanisms of platelet adhesion and aggregation may vary with location in the body depending on the local shear environment. The elucidation of the molecular mechanisms responsible for platelet adhesion and aggregation to extracellular matrix components under flow conditions that simulate those found in vivo is, therefore, very important medically.
Dynamic Bacterial Adhesion to Collagen. Go to The Whitaker Foundation for abstract and specific aims.
Receptor-Mediated Bacterial Adhesion to Extracellular Matrix. Go to National Science Foundation for abstract.
Ross, J. M., "Cellular-extracellular matrix interactions", Frontiers in tissue engineering, eds. Patrick, C. W., Mikos, A.G. and McIntire, L. V., Elsevier science (in press).(/P>
Ross, J. M., Alevriadou, B. R., McIntire L. V., "Rheology", Thrombosis and hemorrhage, 2nd edition, eds. Loscalzo, J., and Schafer, A. I. Williams and Wilkens (in press).
Ross, J. M., McIntire L. V., Moake, J. L., Kuo, Huey-Ju, Quin, R-Q, Glanville, R. W., Schwartz, E., and Rand J.H., "Fibrilin containing elastic microfibrils support platelet adhesion under dynamic shear conditions", Thromb. Haemost. (in press).
J.M. Ross, L.V. McIntire, J.L. Moake and J.H. Rand, "Molecular Mechanisms of Platelet Adhesion and Aggregation on Human Type VI Collagen Surfaces Under Physiological Flow Conditions," Blood, 85, 1826-1835 (1995).abstract
J.M. Ross and L.V. McIntire, "Molecular Mechanisms of Mural Thrombosis Under Dynamic Flow Conditions," News Physiol. Sci, 10, 117-122 (1995). abstract
J. M. Ross, L.V. McIntire, J.L. Moake and J.H. Rand., "The Role of GPIb and GPIIb-IIIa in Platelet Adhesion and Aggregation on Collagen VI Surfaces Under Physiological Flow Conditions, Proceedings of the 3rd International Symposium on Biofluid Mechanics, (1994). abstract
B.F. Roettger, J.A. Myers, M.R. Ladisch and F.E. Regnier, "Adsorption Phenomena in Hydrophobic Interaction Chromatography," Biotechnol. Prog., 5, 79-88 (1989). abstract
Last updated August 1997
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