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Your search keyword '"Kwak, Brenda R."' showing total 12 results
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12 results on '"Kwak, Brenda R."'

1. Artery-Associated Sympathetic Innervation Drives Rhythmic Vascular Inflammation of Arteries and Veins

Author

de Juan, Alba, Ince, Louise Madeleine, Pick, Robert, Chen, Chien-Sin, Molica, Filippo, Zuchtriegel, Gabriele, Wang, Chen, Zhang, Dachuan, Druzd, David, Hessenauer, Maximilian E.T., Pelli, Graziano, Kolbe, Isa, Oster, Henrik, Prophete, Colette, Hergenhan, Sophia Martina, Albrecht, Urs, Ripperger, Jürgen, Montanez, Eloi, Reichel, Christoph A., Soehnlein, Oliver, Kwak, Brenda R., Frenette, Paul S., and Scheiermann, Christoph

Published
2019
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2. Connexin 37 limits thrombus propensity by downregulating platelet reactivity

Author

Angelillo-Scherrer Anne, Fontana Pierre, Burnier Laurent, Roth Isabelle, Sugamele Rocco, Brisset Anne, Morel Sandrine, Nolli Séverine, Sutter Esther, Chassot Alexandra, Capron Claude, Borgel Delphine, Saller François, Chanson Marc, Kwak Brenda R, Waltenberger Johannes, Weber Christian, and Tokgözoglu Lale

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Bleeding Time, Adolescent, Megakaryocytes/physiology, Connexin, Blood Platelets/physiology, 030204 cardiovascular system & hematology, ddc:616.07, 03 medical and health sciences, Biotin/analogs & derivatives/pharmacokinetics, Mice, Young Adult, 0302 clinical medicine, Bleeding time, Platelet Aggregation/physiology, Physiology (medical), Down-Regulation/physiology, medicine, Connexins/genetics/physiology, Animals, Humans, Platelet, Thrombus, ddc:612, Microinjection, 030304 developmental biology, ddc:616, 0303 health sciences, medicine.diagnostic_test, business.industry, Genetic Predisposition to Disease/genetics, Gap junction, medicine.disease, Mice, Mutant Strains, Thrombosis/genetics/physiopathology, Cell biology, Mice, Inbred C57BL, Gap Junctions/physiology, Hemostasis, Polymorphism, Genetic/physiology, Cardiology and Cardiovascular Medicine, business, Intracellular
Abstract

Background— Formation of platelet plug initiates hemostasis after vascular injury and triggers thrombosis in ischemic disease. However, the mechanisms leading to the formation of a stable thrombus are poorly understood. Connexins comprise a family of proteins that form gap junctions enabling intercellular coordination of tissue activity, a process termed gap junctional intercellular communication . Methods and Results— In the present study, we show that megakaryocytes and platelets express connexin 37 (Cx37). Deletion of the Cx37 gene in mice shortens bleeding time and increases thrombus propensity. Aggregation is increased in murine Cx37 −/− platelets or in murine Cx37 +/+ and human platelets treated with gap junction blockers. Intracellular microinjection of neurobiotin, a Cx37-permeant tracer, revealed gap junctional intercellular communication in platelet aggregates, which was impaired in Cx37 −/− platelets and in human platelets exposed to gap junction blockers. Finally, healthy subjects homozygous for Cx37–1019C, a prognostic marker for atherosclerosis, display increased platelet responses compared with subjects carrying the Cx37–1019T allele. Expression of these polymorphic channels in communication-deficient cells revealed a decreased permeability of Cx37–1019C channels for neurobiotin. Conclusions— We propose that the establishment of gap junctional communication between Cx37-expressing platelets provides a mechanism to limit thrombus propensity. To our knowledge, these data provide the first evidence incriminating gap junctions in the pathogenesis of thrombosis.

Published
2011
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9. Role of Endogenous Fas (CD95/Apo-1) Ligand in Balloon-Induced Apoptosis, Inflammation, and Neointima Formation

Author

Matter, Christian M., primary, Chadjichristos, Christos E., additional, Meier, Patricia, additional, von Lukowicz, Tobias, additional, Lohmann, Christine, additional, Schuler, Pia K., additional, Zhang, Dongming, additional, Odermatt, Bernhard, additional, Hofmann, Eugen, additional, Brunner, Thomas, additional, Kwak, Brenda R., additional, and Lüscher, Thomas F., additional

Published
2006
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