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Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart
文献类型：期刊论文
| 作者 | He, LJ; Liu, QZ; Hu, TY; Huang, XZ; Zhang, H; Tian, XY; Yan, Y; Wang, L; Huang, Y; Miquerol, L |
| 刊名 | CARDIOVASCULAR RESEARCH
 |
| 出版日期 | 2016 |
| 卷号 | 109期号:3页码:419-430 |
| 关键词 | FEMORAL-ARTERY OCCLUSION ENDOTHELIAL-CELLS CORONARY-ARTERIES TRANSGENIC MOUSE RABBIT HINDLIMB CRE-RECOMBINASE IN-VIVO APELIN ANGIOGENESIS MICE |
| 通讯作者 | Zhou, B (reprint author), Chinese Acad Sci, Grad Sch, Shanghai Inst Biol Sci, Key Lab Nutr & Metab,Inst Nutr Sci, Shanghai 200031, Peoples R China. ; Zhou, B (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, CAS Ctr Excellence Brain Sci & Intelligence Techn, Inst Neurosci,State Key Lab Neurosci, Shanghai 200031, Peoples R China. ; Zhou, B (reprint author), ShanghaiTech Univ, Shanghai 201210, Peoples R China.,zhoubin@sibs.ac.cn |
| 英文摘要 | Capillary and arterial endothelial cells share many common molecular markers in both the neonatal and adult hearts. Herein, we aim to establish a genetic tool that distinguishes these two types of vessels in order to determine the cellular mechanism underlying collateral artery formation. Using Apln-GFP and Apln-LacZ reporter mice, we demonstrate that APLN expression is enriched in coronary vascular endothelial cells. However, APLN expression is reduced in coronary arterial endothelial cells. Genetic lineage tracing, using an Apln-CreER mouse line, robustly labelled capillary endothelial cells, but not arterial endothelial cells. We leveraged this differential activity of Apln-CreER to study collateral artery formation following myocardial infarction (MI). In a neonatal heart MI model, we found that Apln-CreER-labelled capillary endothelial cells do not contribute to the large collateral arteries. Instead, these large collateral arteries mainly arise from pre-existing, infrequently labelled coronary arteries, indicative of arteriogenesis. Furthermore, in an adult heart MI model, Apln-CreER activity also distinguishes large and small diameter arteries from capillaries. Lineage tracing in this setting demonstrated that most large and small coronary arteries in the infarcted myocardium and border region are derived not from capillaries, but from pre-existing arteries. Apln-CreER-mediated lineage tracing distinguishes capillaries from large arteries, in both the neonatal and adult hearts. Through genetic fate mapping, we demonstrate that pre-existing arteries, but not capillaries, extensively contribute to collateral artery formation following myocardial injury. These results suggest that arteriogenesis is the major mechanism underlying collateral vessel formation. |
| WOS标题词 | Cardiovascular System & Cardiology |
| 学科主题 | Cardiac & Cardiovascular Systems |
| 语种 | 英语 |
| WOS记录号 | WOS:000371521100011 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/4035]  |
| 专题 | 上海神经科学研究所_神经所(总) |
| 推荐引用方式 GB/T 7714 | He, LJ,Liu, QZ,Hu, TY,et al. Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart[J]. CARDIOVASCULAR RESEARCH,2016,109(3):419-430. |
| APA | He, LJ.,Liu, QZ.,Hu, TY.,Huang, XZ.,Zhang, H.,...&Zhou, B.(2016).Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart.CARDIOVASCULAR RESEARCH,109(3),419-430. |
| MLA | He, LJ,et al."Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart".CARDIOVASCULAR RESEARCH 109.3(2016):419-430. |
入库方式： OAI收割
来源：上海神经科学研究所
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