دورية أكاديمية

Murine sca1/flk1-positive cells are not endothelial progenitor cells, but B2 lymphocytes

التفاصيل البيبلوغرافية
العنوان: Murine sca1/flk1-positive cells are not endothelial progenitor cells, but B2 lymphocytes
المؤلفون: Steffen, Eva, Mayer von Wittgenstein, Wolfgang Bernd Edziu, Hennig, Marie, Niepmann, Sven Thomas, Zietzer, Andreas, Werner, Nikos, Rassaf, Tienush, Nickenig, Georg, Wassmann, Sven, Zimmer, Sebastian, Steinmetz, Martin
المصدر: http://lobid.org/resources/99370671625606441Test#!, 115(2):18.
سنة النشر: 2020
المجموعة: Publisso (ZB MED-Publikationsportal Lebenswissenschaften)
مصطلحات موضوعية: Endothelial Progenitor Cells/metabolism [MeSH], Antigens, Ly/genetics [MeSH], Endothelial regeneration, Mice, Inbred C57BL [MeSH], Original Contribution, Atherosclerosis, DNA-Binding Proteins/deficiency [MeSH], B-Lymphocyte Subsets/pathology [MeSH], Lymphocyte Depletion [MeSH], Atherosclerosis/pathology [MeSH], DNA-Binding Proteins/genetics [MeSH], Carotid Artery Injuries/metabolism [MeSH], Male [MeSH], Membrane Proteins/metabolism [MeSH], Phenotype [MeSH], Atherosclerosis/metabolism [MeSH], Carotid Artery, Common/immunology [MeSH], Disease Models, Animal [MeSH], Endothelial Progenitor Cells/immunology [MeSH], Vascular Endothelial Growth Factor Receptor-2/metabolism [MeSH], Membrane Proteins/genetics [MeSH], Carotid Artery Injuries/pathology [MeSH], Female [MeSH], Vascular Endothelial Growth Factor Receptor-2/genetics [MeSH], Cell Proliferation [MeSH], Endothelial dysfunction
الوصف: Heart failure is a major health problem worldwide with a significant morbidity and mortality rate. Although studied extensively in animal models, data from patients at the compensated disease stage are lacking. We sampled myocardium biopsies from aortic stenosis patients with compensated hypertrophy and moderate heart failure and used transcriptomics to study the transition to failure. Sequencing and comparative analysis of analogous samples of mice with transverse aortic constriction identified 25 candidate genes with similar regulation in response to pressure overload, reflecting highly conserved molecular processes. The gene cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) is upregulated in the transition to failure in human and mouse and its function is unknown. Homology to ion channel regulatory toxins suggests a role in Ca
نوع الوثيقة: article in journal/newspaper
اللغة: English
ردمك: 978-9937-0-6716-4
9937-0-6716-2
العلاقة: https://repository.publisso.de/resource/frl:6466436Test; https://doi.org/10.1007/s00395-020-0774-6Test; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981106Test/
DOI: 10.1007/s00395-020-0774-6
الإتاحة: https://doi.org/10.1007/s00395-020-0774-6Test
https://repository.publisso.de/resource/frl:6466436Test
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981106Test/
حقوق: https://creativecommons.org/licenses/by/4.0Test/
رقم الانضمام: edsbas.D4AD11B7
قاعدة البيانات: BASE
الوصف
ردمك:9789937067164
9937067162
DOI:10.1007/s00395-020-0774-6