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2 results on '"Zhong TP"'

1. Subepicardial endothelial cells invade the embryonic ventricle wall to form coronary arteries

Author

Adriana C. Gittenberger-de Groot, Zhongzhou Yang, Sylvia M. Evans, Xueying Tian, Bin Zhou, Wei Yu, Qiaozhen Liu, Zhen Zhang, Robert J. Schwartz, Zhen Yang, Xiuzhen Huang, Lingjuan He, Jie Lu, Yan Yan, Tao P. Zhong, Kristy Red-Horse, Hui Zhang, Antonio Baldini, Tianyuan Hu, Yunfu Sun, Liang He, Xiao Yang, Tian, X, Hu, T, Zhang, H, He, L, Huang, X, Liu, Q, Yu, W, Yang, Z, Zhang, Z, Zhong, Tp, Yang, X, Yan, Y, Baldini, Antonio, Sun, Y, Lu, J, Schwartz, Rj, Evans, Sm, Gittenberger de Groot, Ac, Red Horse, K, and Zhou, B.

Subjects
medicine.medical_specialty, coronary artery, Heart Ventricles, Neovascularization, Physiologic, Biology, Mice, angiogenesis, Internal medicine, origin, medicine, Animals, Gene Knock-In Techniques, Atrium (heart), development, Molecular Biology, Endocardium, subepicardial endothelial cell, Sinus venosus, Heart development, Myocardium, Endothelial Cells, Heart, Cell Biology, Blood flow, Coronary Vessels, Research Highlight, Mice, Inbred C57BL, Coronary arteries, medicine.anatomical_structure, Ventricle, cardiovascular system, Cardiology, Embryonic Ventricle
Abstract

Coronary arteries bring blood flow to the heart muscle. Understanding the developmental program of the coronary arteries provides insights into the treatment of coronary artery diseases. Multiple sources have been described as contributing to coronary arteries including the proepicardium, sinus venosus (SV), and endocardium. However, the developmental origins of coronary vessels are still under intense study. We have produced a new genetic tool for studying coronary development, an AplnCreER mouse line, which expresses an inducible Cre recombinase specifically in developing coronary vessels. Quantitative analysis of coronary development and timed induction of AplnCreER fate tracing showed that the progenies of subepicardial endothelial cells (ECs) both invade the compact myocardium to form coronary arteries and remain on the surface to produce veins. We found that these subepicardial ECs are the major sources of intramyocardial coronary vessels in the developing heart. In vitro explant assays indicate that the majority of these subepicardial ECs arise from endocardium of the SV and atrium, but not from ventricular endocardium. Clonal analysis of Apln-positive cells indicates that a single subepicardial EC contributes equally to both coronary arteries and veins. Collectively, these data suggested that subepicardial ECs are the major source of intramyocardial coronary arteries in the ventricle wall, and that coronary arteries and veins have a common origin in the developing heart.

Published
2013
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2. Endothelial CDS2 deficiency causes VEGFA-mediated vascular regression and tumor inhibition.

Author

Zhao W, Cao L, Ying H, Zhang W, Li D, Zhu X, Xue W, Wu S, Cao M, Fu C, Qi H, Hao Y, Tang YC, Qin J, Zhong TP, Lin X, Yu L, Li X, Li L, Wu D, and Pan W

Subjects
Animals, Cell Line, Tumor, Diacylglycerol Cholinephosphotransferase genetics, Endothelial Cells enzymology, Humans, Melanoma, Experimental, Mice, Mice, Knockout, Nucleotidyltransferases genetics, Vascular Endothelial Growth Factor A genetics, Zebrafish, Zebrafish Proteins genetics, Diacylglycerol Cholinephosphotransferase physiology, Neoplasms blood supply, Neovascularization, Pathologic genetics, Neovascularization, Physiologic genetics, Nucleotidyltransferases metabolism, Vascular Endothelial Growth Factor A metabolism, Zebrafish Proteins metabolism
Abstract

The response of endothelial cells to signaling stimulation is critical for vascular morphogenesis, homeostasis and function. Vascular endothelial growth factor-a (VEGFA) has been commonly recognized as a pro-angiogenic factor in vertebrate developmental, physiological and pathological conditions for decades. Here we report a novel finding that genetic ablation of CDP-diacylglycerol synthetase-2 (CDS2), a metabolic enzyme that controls phosphoinositide recycling, switches the output of VEGFA signaling from promoting angiogenesis to unexpectedly inducing vessel regression. Live imaging analysis uncovered the presence of reverse migration of the angiogenic endothelium in cds2 mutant zebrafish upon VEGFA stimulation, and endothelium regression also occurred in postnatal retina and implanted tumor models in mice. In tumor models, CDS2 deficiency enhanced the level of tumor-secreted VEGFA, which in-turn trapped tumors into a VEGFA-induced vessel regression situation, leading to suppression of tumor growth. Mechanistically, VEGFA stimulation reduced phosphatidylinositol (4,5)-bisphosphate (PIP2) availability in the absence of CDS2-controlled-phosphoinositide metabolism, subsequently causing phosphatidylinositol (3,4,5)-triphosphate (PIP3) deficiency and FOXO1 activation to trigger regression of CDS2-null endothelium. Thus, our data indicate that the effect of VEGFA on vasculature is context-dependent and can be converted from angiogenesis to vascular regression.

Published
2019
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