کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8475867 | 1550567 | 2016 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
VEGF regulates relative allocation of Isl1+ cardiac progenitors to myocardial and endocardial lineages
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کلمات کلیدی
IB4FLK1SHFPBSOFTISHhpfCPCSGOFSPFLOFIn situ hybridization - Hybridization در محلisl1 - Isl1Loss-of-function - از دست دادن عملکردisolectin B4 - ایزوکتین B4Ventricle - بطن چپspecific pathogen-free - خاص بدون پاتوژنatrium - دهلیزMyosin heavy chain - زنجیره سنگین میوزینCardiac progenitor cells - سلول های پیش از قاعدگیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)Phosphate buffered saline - فسفات بافر شورMHC - مجموعه سازگاری بافتی اصلیOutflow tract - مسیر خروجیSecond heart field - میدان دوم قلبcleaved caspase-3 - کاسیاس شکسته 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
A fundamental issue in organogenesis is how dichotomous fate decisions are made securing proper allocation of multipotent progenitors to their respective descendants. Previous lineage tracing analyses showing Isl1+/VEGFR2+ cardiac progenitors in the second heart field give rise to both endocardium and myocardium suggest VEGF plays a role in this fate decision, conceivably promoting an endocardial fate. Isl1+ multipotent progenitors and lineage-committed descendants thereof were visualized and quantified within their transition zone in the outflow tract. Forced VEGF expression during the critical E8.5-E10.5 interval tilted the balance between myocardial- and endocardial-committed progenitors towards the latter, culminating in generation of surplus endocardium developing at the expense of a much thinner myocardium. Experiments ruled-out that surplus endocardium is due to VEGF-induced endocardial proliferation and that reduced myocardium is due to myocardial apoptosis. Inducing VEGF after most Isl1+ progenitors have been exhausted had no effect on the normal endocardia/myocardial ratio but instead produced an unrelated coronary phenotype. Together, these results uncover a novel role for VEGF in controlling proper allocation of Isl1+ cardiac progenitors to their respective descending lineages.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mechanisms of Development - Volume 142, November 2016, Pages 40-49
Journal: Mechanisms of Development - Volume 142, November 2016, Pages 40-49
نویسندگان
Zhiheng He, Myriam Grunewald, Yuval Dor, Eli Keshet,