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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

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Using a GFP-tagged TMEM184A Construct for Confirmation of Heparin Receptor Identity
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Profiling heparin-chemokine interactions using synthetic tools.

Jose L de Paz1, E Ashley Moseman, Christian Noti

  • 1Laboratory for Organic Chemistry, Swiss Federal Institute of Technology (ETH) Zürich, Wolfgang-Pauli-Strasse 10, HCI F315, 8093 Zürich, Switzerland.

ACS Chemical Biology
|November 23, 2007
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Glycosaminoglycans (GAGs) are vital for chemokine function in cell migration. Specific heparin sequences binding chemokines were identified, leading to synthetic dendrimers that block lymphocyte homing to inflammatory sites.

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Engineering Antiviral Agents via Surface Plasmon Resonance
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Area of Science:

  • Immunology
  • Glycobiology
  • Molecular Biology

Background:

  • Chemokines are crucial for leukocyte trafficking and inflammation.
  • Glycosaminoglycans (GAGs), like heparin, are essential for chemokine function in vivo.
  • Understanding GAG-chemokine interactions is key to modulating immune responses.

Purpose of the Study:

  • To characterize the heparin binding profiles of eight key chemokines.
  • To identify specific GAG sequences involved in chemokine binding.
  • To investigate the potential of synthetic GAG structures in modulating chemokine-mediated cell migration.

Main Methods:

  • Utilized heparin microarrays with synthetic heparin oligosaccharides to assess chemokine binding.
  • Validated binding data using surface plasmon resonance (SPR).
  • Performed in vitro chemotaxis and homing assays using GAG-coated dendrimers.

Main Results:

  • Chemokines exhibited distinct heparin binding profiles; CCL21 strongly bound a specific hexasaccharide, while CCL19 and CXCL12 showed weak or no binding.
  • Synthetic heparin dendrimers, when coated with a specific sulfated hexasaccharide, inhibited lymphocyte migration towards CCL21.
  • Lymphocyte migration towards CXCL12 and CCL19 was unaffected by the dendrimers, suggesting specific GAG-chemokine interactions dictate migration patterns.

Conclusions:

  • Specific GAG sequences mediate differential chemokine binding and subsequent leukocyte migration.
  • Synthetic heparin dendrimers can selectively block chemokine-driven lymphocyte homing by disrupting GAG-chemokine gradient formation.
  • These findings provide a foundation for developing novel therapeutics targeting GAG-chemokine interactions to control immune cell trafficking.