Leukocyte Bim deficiency does not impact atherogenesis in ldlr −/− mice, despite a pronounced induction of autoimmune inflammation

Autor: Lieve Temmerman, Marijke M. Westra, Ilze Bot, Bart J. M. van Vlijmen, Niek van Bree, Martine Bot, Kim L. L. Habets, Tom G. H. Keulers, Johan van der Vlag, Thomas G. Cotter, Theo J. C. van Berkel, Erik A. L. Biessen

Publikováno v: Scientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)

Abstract Proapoptotic Bcl-2 family member Bim is particularly relevant for deletion of autoreactive and activated T and B cells, implicating Bim in autoimmunity. As atherosclerosis is a chronic inflammatory process with features of autoimmune disease

Externí odkaz: https://doaj.org/article/03205742549a4e9196533178b4a8d0fd

Low human and murine Mcl-1 expression leads to a pro-apoptotic plaque phenotype enriched in giant-cells

Autor: Saskia C. A. de Jager, Erik A.L. Biessen, Ilze Bot, Lieve Temmerman, You-Wen He, Marion J.J. Gijbels, Ivan Dzhagalov, Theo J.C. Van Berkel, Chris P. M. Reutelingsperger, Margaux A.C. Fontaine, Marijke M. Westra, Martine Bot, Judith C. Sluimer, Han Jin, Aimee Franssen, Bart J.M. van Vlijmen

Publikováno v: Scientific Reports, 9(1). Nature Publishing Group
Scientific Reports, Vol 9, Iss 1, Pp 1-11 (2019)
Scientific Reports, 9(1), 14547
Scientific Reports, 9:14547. Nature Publishing Group
Scientific Reports
Scientific Reports, 9. NATURE PUBLISHING GROUP
Scientific reports, 9(1):14547. Nature Publishing Group

The anti-apoptotic protein myeloid cell leukemia 1 (Mcl-1) plays an important role in survival and differentiation of leukocytes, more specifically of neutrophils. Here, we investigated the impact of myeloid Mcl-1 deletion in atherosclerosis. Western

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::82d3254ac320b1b7852306cd5ee57bce
https://dspace.library.uu.nl/handle/1874/389288

Leukocyte Bim deficiency does not impact atherogenesis in ldlr

Autor: Lieve, Temmerman, Marijke M, Westra, Ilze, Bot, Bart J M, van Vlijmen, Niek, van Bree, Martine, Bot, Kim L L, Habets, Tom G H, Keulers, Johan, van der Vlag, Thomas G, Cotter, Theo J C, van Berkel, Erik A L, Biessen

Publikováno v: Scientific Reports

Proapoptotic Bcl-2 family member Bim is particularly relevant for deletion of autoreactive and activated T and B cells, implicating Bim in autoimmunity. As atherosclerosis is a chronic inflammatory process with features of autoimmune disease, we inve

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::7bfbdaa3e34f1096c99553392ae8da8c
https://pubmed.ncbi.nlm.nih.gov/28596542

Abstract 459: Vascular Neuropeptide Y Contributes to Atherosclerotic Plaque Progression and Perivascular Mast Cell Activation

Autor: H Maxime Lagraauw, Marijke M Westra, Martine Bot, Anouk Wezel, Peter J Santbrink, Gerard Pasterkamp, Erik A Biessen, Johan Kuiper, Ilze Bot

Publikováno v: Arteriosclerosis, Thrombosis, and Vascular Biology. 34

Aim: Neuropeptide Y is an abundantly expressed neurotransmitter capable of modulating both immune and metabolic responses related to the development of atherosclerosis. NPY receptors are expressed by a number of vascular wall cell types, among which

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::467abd79aca7263774aff2443f986b77
https://doi.org/10.1161/atvb.34.suppl_1.459

Abstract 1947: Chymase Inhibition Reduces the Incidence of Intraplaque Hemorrhage and Induces a Stable Atherosclerotic Plaque Phenotype in ApoE Deficient Mice

Autor: Ilze Bot, Marijke M Westra, Sandra H van Heiningen, Hans Hilpert, Inge M Lankhuizen, Theo J van Berkel, Jürgen Fingerle, Erik A Biessen

Publikováno v: Circulation. 118

Mast cells are abundantly present in perivascular tissue during atherosclerotic plaque progression and were previously demonstrated to contribute significantly to plaque destabilization. In this study, we aimed to investigate to what extent inhibitio

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::f16a49fdf6e1440b3a915e9180666626
https://doi.org/10.1161/circ.118.suppl_18.s_410