Abstract | 第5-7页 |
中文摘要 | 第8-10页 |
Abbreviation | 第10-12页 |
Chapter 1 A Brief Review:Cardiac valve development is determined by both genetic andenvironmental factors | 第12-50页 |
1. Function of cardiac valve in vertebrates and significance of valve development research | 第13-16页 |
1.1 Structure of mature valve | 第13-14页 |
1.2 Function of valve | 第14-15页 |
1.3 Congenital valve diseases and cues | 第15-16页 |
2. Developmental procedures of valve morphogenesis | 第16-26页 |
2.1 Valve development in amniotic vertebrate | 第16-19页 |
2.2 Valve generation in zebrafish | 第19-26页 |
3. Regulatory control of valvulogenesis | 第26-33页 |
3.1 Epigenetic factors impact early cardiac and valve formation | 第26-27页 |
3.2 Genetic factors participate in valve development | 第27-33页 |
4. Research progresses in the effect of nitrite and retinoic acid on vertebrate cardiac development and valve formation | 第33-44页 |
4.1 Research progresses in the effect of nitrite on vertebrate cardiac development and valve formation | 第33-39页 |
4.2 Research progresses in the effect of retinoic acid signaling on vertebrate cardiac development and valve formation | 第39-44页 |
References | 第44-50页 |
Chapter 2 The role of sodium nitrite in cardiac valve formation of zebrafish embryos | 第50-80页 |
Summary | 第51-52页 |
Introduction | 第52-54页 |
Materials and Methods | 第54-60页 |
Results | 第60-75页 |
1. Exposure of sodium nitrite induces pericardial edema of zebrafish embryos in a dose-and time-dependent way | 第60-62页 |
2. Sodium nitrite exposure does not impact early stages of cardiac development in zebrafish embryos | 第62-64页 |
3. Sodium nitrite impacts later valve formation | 第64-67页 |
4. Sodium nitrite exposure does not impact hemodynamics of zebarfish early embryos | 第67-69页 |
5. Generation of cardiac valve progenitor cells are impacted by overdosing sodium nitrite | 第69-70页 |
6. Loss of flk1 positive cell accumulation in atrio-ventricular canal | 第70-71页 |
7. Reducing NO signaling can rescue the abnormal heart defect induced by overdosing nitrite | 第71-73页 |
8: Low concentration of oxygen in ambient water accelerates malformation of zebrafish heart development induced by sodium nitrite exposure | 第73-75页 |
Discussion | 第75-78页 |
References | 第78-80页 |
Chapter 3 Retinoic acid signaling is required for zebrafish valvulogenesis | 第80-111页 |
Summary | 第81-82页 |
Intrioducntion | 第82-85页 |
Method and material | 第85-89页 |
Results | 第89-104页 |
1. Lower concentration of aldh1α2 morpholino causes specific cardiac edema rather than malformation of many other tissues | 第89-91页 |
2. Appropriate RA level in vivo is required for AVC valve leaflets formation of zebra fish embryos | 第91-93页 |
3. The effect of RA signaling on cardiac progenitor pool is not the reason for RA deficiency induced cardiac edema | 第93-94页 |
4. Earlier stages of cardiac development, before valve formation, are not disrupted in aldh1α2 morphants | 第94-96页 |
5. Hemodynamics elements, required for valve formation, are not changed under decreased RA signaling condition | 第96-98页 |
6. Invagination of endothelial cells in AVC is sensitive to endogenous RA signaling level | 第98-99页 |
7. Induction of earliest myocardial genes and specification of myocardial AVC do not require endogenous RA signaling maintain | 第99-101页 |
8. Expression of endocardial genes in AVC, required for endocardial cushion formation, are disrupted by insufficient RA signaling supply | 第101-102页 |
9. Loss of expression pattern of endocardial markers in aldh1α2 morphants can be rescued by RA addition | 第102-104页 |
Discussion | 第104-107页 |
Reference | 第107-111页 |
致谢 | 第111-112页 |
Publication | 第112-114页 |