Thrombosis Research Areas

Areas of Interest

• Animal models of thrombosis (Leng, López, Bray, Gushiken, Smith)
• Antiphospholipid antibodies (Gushiken, Thiagarajan, Teruya)
• Clinical Trials in Thrombosis/Hemostasis (Hoots, Kleiman, Muntz, Rice, Baker)
• Endothelial cell biology (Berndt, Durante)
• Genetic epidemiology (Bray, Afsharkharghan, López)
• Hemophilia (Hoots, Baker, Rice)
• Hormonal effects on platelets (Leng, Bray)
• Hypercoagulability (Bray, Afsharkharghan, Gushiken, Baker, Moake, Thiagarajan, Kroll, Rice, Hoots, Muntz)
• Leukocyte biology (Smith, López, Afsharkharghan, Berndt, Dong)
• Platelet adhesion (López, Dong, Cruz, Berndt, Kroll, McIntire, Shrimpton)
• Platelet aggregation (Bray, Dong, Gushiken)
• Platelet biochemistry (Cruz, López)
• Platelet integrins (Bray, Cruz, Vijayan)
• Platelet polymorphisms (Afsharkharghan, Bray, López, Vijayan)
• Platelet signaling (Kroll, Bray, Vijayan, Berndt, Dong, Shrimpton, Gushiken)
• Rheology (McIntire, Dong, López, Kroll, Cruz, Moake)
• Thrombotic thrombocytopenic purpura (TTP) (Moake, McIntire, Baker, Rice)
• Von Willebrand factor (Cruz, Berndt, Moake, McIntire, Dong, Hoots)
• Coagulation factors (Hoots, Thiagarajan, Teruya)
• Diagnostics (Teruya, Bray)

Specialized Laboratories

The Platelet Shear and Flow Cytometry Laboratory is located on the 13th floor of the Alkek Research Building. This is a state-of-the-art facility for the evaluation of the effects of shear force on cell adhesion and physiology. This facility has a parallel plate flow chamber with real-time video-microscopy and a hi speed (3,600 frames/minute) digital camera, a Nikon Eclipse TE300 inverted stage fluorescence microsope (with filters for FITC, PE, pH, fura-2), a Nikon E800 upright microscope, a HAAKE RheoStress I (RSI) Rheometer (viscometer) and a BioRad Fluorometer.

The Fondren Vascular Biology and Thrombosis Core Laboratory is part of the Athero-Thrombosis Laboratory dedicated to clinical/translational research in the area of occlusive vascular disease. The Thrombosis Core Laboratory has an ABI Prism 7700 Sequence Detector (real-time PCR), Dade-Behring BCS Coagulation Analyzer, a Beckman-Coulter EPICS XL-MCL flow cytometer, a HAAKE RheoStress I (RSI) Rheometer (viscometer), 2 BIO-DATA 4-channel platelet PAP-4D aggregometers, a Coulter Z2 Particle Counter, a Dade-Behring PFA-100, and an MJ Research PTC-100 PCR machine.

Specialized Center of Research (SCOR) Laboratories

Platelets, Shear Stress, and Arterial Thrombosis

RESPONSIBLE INVESTIGATOR:

José A. López, M.D.

OTHER INVESTIGATORS:

Jing-fei Dong, M.D., Ph.D.
Michael Berndt, Ph.D.

.The overall objective of this project is to define the precise sequences within GP Iba (the ligand-binding subunit of the GP Ib-IX-V complex) involved in its interaction with vWf and to investigate the mechanism by which shear stress induces this interaction.

Molecular Mechanism of Shear-Induced Platelet Activation

RESPONSIBLE INVESTIGATOR:

Michael Kroll, M.D.

OTHER INVESTIGATORS:

Andrew I. Schafer, M.D.
Michael Berndt, Ph.D.

The overall objective of this project is to investigate the initial sensing of shear stress by platelets, a process that may "prime" the GP Ib-IX-V complex to bind vWf, and the proximal intracellular signals transmitted subsequent to that binding.

Genetic Variation Affecting the GPIb-IX/IIb-IIIa Axis

RESPONSIBLE INVESTIGATOR:

Paul F. Bray, M.D.

OTHER INVESTIGATORS:

José A. López, M.D.
Jing-fei Dong, M.D., Ph.D.
Vinod Vijayan, Ph.D.
Perumal Thiagarajan, M.D.

The overall objective of this project is to explore the relationship between observed differences in post-occupancy signaling and genetic variation in the two major platelet adhesion receptors, the GP Ib-IX-V complex and integrin aIIbb3 (GP IIb-IIIa).

Endothelial Cells, vWF Cleavage, and Thrombotic Microangiopathies

RESPONSIBLE INVESTIGATOR:

Joel C. Moake, M.D.

OTHER INVESTIGATORS:

Michael Berndt, Ph.D.
Larry McIntire, Ph.D.

The overall objective of this project is to 1) examine the requirements of a plasma metalloprotease for cleaving ultra-large (UL) forms of vWf, 2) evaluate whether the UL multimers of vWf that are responsible for most cases of sporadic and chronic relapsing thrombotic thrombocytopenic purpura TTP are also the proximal causative agents of other forms of acquired TTP, and 3) evaluate the potential for using agents that block vWf binding to platelets as agents to treat refractory TTP.

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