CXCR7‐agonist countered activation induced externalisation of thrombogenic phosphatidylserine, thus checked PRP but not plasma dependent (PPP) thrombin generation, or efficiency of clot formation, stabilisation and dissolution.
The pharmacological CXCR7‐agonist, counteracted GPVI‐PAR1‐P2Y12 induced degranulation, αIIbβIII‐integrin activation, aggregation, ex vivo thrombus formation in healthy subjects, STEMI patients and mice, reduced the rate and extent of platelet interaction with collagen, fibrinogen, ROS generation, the release of thromboinflammatory arachidonic acid, thromboxane A2, 12‐HETE, HHT. Results: Deletion of CXCR7 from platelets in Pf4‐Cre + CXCR7 flox/flox mice led to enhanced thrombotic disposition without affecting haemostasis. Methods: Flowcytometry, thrombinoscopy, thromboelastography, bleeding time, flow chamber assay, intravital microscopy, mass spectrometry, live imaging by scanning ion conductance microscopy. Gawaz 1ġUniversity Clinic of Tübingen, Department of Cardiology and Cardiovascular Diseases, Tübingen, Germany, 2University of Tübingen, Institute of Pharmaceutical Sciences, Tübingen, Germany, 3University of Tübingen, Institute of Applied Physics, Tübingen, Germanyīackground: Elevated platelet surface expression of the chemokine CXCL12 and its receptors CXCR4‐CXCR7 in acute coronary syndrome influences functional recovery and prognosis.Īims: This study explores the anti‐thrombotic potential of CXCR7 and its effects on thromboinflammation.
PB001: Platelet Chemokine Receptor CXCR7 Mediates an Anti‐thrombotic and Anti‐thromboinflammatory Effect
0 kommentar(er)
