Conditional knockout of activin like kinase-1 (ALK-1) leads to heart failure without maladaptive remodeling
| العنوان: | Conditional knockout of activin like kinase-1 (ALK-1) leads to heart failure without maladaptive remodeling |
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| المؤلفون: | Lyanne Buiten, Richard H. Karas, Prerna Nepali, Emily E. Mackey, Mark Aronovitz, Jonathan Levine, Robert M. Blanton, Keshan Ughreja, Xiaoying Qiao, Navin K. Kapur, S. Paul Oh, Kevin J. Morine, Vikram Paruchuri |
| المصدر: | Heart and Vessels. 32:628-636 |
| بيانات النشر: | Springer Science and Business Media LLC, 2017. |
| سنة النشر: | 2017 |
| مصطلحات موضوعية: | 0301 basic medicine, endocrine system, medicine.medical_specialty, Cardiac fibrosis, Activin Receptors, Type II, 030204 cardiovascular system & hematology, Real-Time Polymerase Chain Reaction, Ventricular Function, Left, Article, Contractility, 03 medical and health sciences, 0302 clinical medicine, hemic and lymphatic diseases, Internal medicine, Conditional gene knockout, Animals, Medicine, Alleles, High-output heart failure, Heart Failure, Mice, Knockout, Ventricular Remodeling, business.industry, Endoglin, medicine.disease, CTGF, Disease Models, Animal, 030104 developmental biology, Blood pressure, Endocrinology, Gene Expression Regulation, Heart failure, Disease Progression, RNA, Cardiology and Cardiovascular Medicine, business, Activin Receptors, Type I, Signal Transduction |
| الوصف: | Activin like kinase-1 (AlK-1) mediates signaling via the transforming growth factor beta (TGFβ) family of ligands. AlK-1 activity promotes endothelial proliferation and migration. Reduced AlK-1 activity is associated with arteriovenous malformations. No studies have examined the effect of global AlK-1 deletion on indices of cardiac remodeling. We hypothesized that reduced levels of AlK-1 promote maladaptive cardiac remodeling. To test this hypothesis, we employed AlK-1 conditional knockout mice (cKO) harboring the ROSA26-CreER knock-in allele, whereby a single dose of intraperitoneal tamoxifen triggered ubiquitous Cre recombinase-mediated excision of floxed AlK-1 alleles. Tamoxifen treated wild-type (WT-TAM; n = 5) and vehicle treated AlK-1-cKO mice (cKO-CON; n = 5) served as controls for tamoxifen treated AlK-1-cKO mice (cKO-TAM; n = 15). AlK-1 cKO-TAM mice demonstrated reduced 14-day survival compared to cKO-CON controls (13 vs 100%, respectively, p |
| تدمد: | 1615-2573 0910-8327 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::badfc4a25d68c24406648d380b2ee559Test https://doi.org/10.1007/s00380-017-0955-xTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....badfc4a25d68c24406648d380b2ee559 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 16152573 09108327 |
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