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 |