2014 Group Project 5

2014 Student Projects
2014 Student Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7 | Group 8
The Group assessment for 2014 will be an online project on Fetal Development of a specific System. This page is an undergraduate science embryology student and may contain inaccuracies in either description or acknowledgements.

Cardiovascular

--Mark Hill (talk) 15:16, 26 August 2014 (EST) OK you have some headings, how about some content, references, sources for each section. See Lab 3 Assessment.

--Mark Hill (talk) 11:48, 6 September 2014 (EST) This is a start. Less textbook referencing please, more research/reviews from the published literature. Textbooks should not be used as primary sources, I am happy for them to be listed as related literature.

Introduction

• The cardiovascular system is one of the first systems to function within the embryo
• The heart begins to function during the 4th week

[Textbook- Larsen's Human Embryology, 4th ed.]

Timeline

--Z3418340 (talk) 00:21, 27 August 2014 (EST)

(From Textbook- Larsen's Human Embryology, 4th ed. - http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-0-443-06811-9..10012-0&isbn=978-0-443-06811-9&uniqId=462162262-2#4-u1.0-B978-0-443-06811-9..10012-0--fig42)

Primordial heart tube

• Arises predominantly from splanchnic mesoderm in the cardiogenic region
• Initially bilateral, the cardiogenic region cranially merges to form a horseshoe
• During the third week (Approximately day 18), angioblastic chords develop in the cardiogenic mesoderm. It forms the bilateral endocardial heart tubes
• Lateral folding of the embryo brings the heart tubes into the ventral midline.
• Fusion of the heart begins cranially and extends caudally.
• Certain dilations appear in the heart tube including:
  • Truncus arteriosus
  • Bulbus cordis
  • Primordial ventricle
  • Primordial atrium
  • Sinus venosus (further divided into right horn and left horn)

Heart tube looping

• Most looping occurs in the fourth week of development and is completed by the fifth.
• The straight heart tube begins to elongate, most notably with growth in the bulbus cordis and primitive ventricle.
• This causes the heart to bend ventrally and rotate to the right- this forms a C-shaped loop.
• The ventricular bend moves caudally. The distance between outflow and inflow tracts diminishes
• The inflow (atrial) and outflow tracts converge. Myocardial cells are added forming the truncus arteriosus.

Current Research

• Neural crest cells are required for correct positioning of the developing outflow cushions and pattern the arterial valve leaflets: Neural crest cells (NCC) are indicated to be essential at earlier stages of arterial valve development than previously documented, crucially influencing the site of outflow cushions, and patterning the valve leaflets. The data indicates that the dispersal of NCC’s in the unseptated outflow tract establishes the pattern of valve leaflets produced after outflow septation has occurred. Anomalies in NCC adhesion or communication results in disordered NCC condensation at the primary stages of outflow cushion development leading to malpositioned outflow cushions. These findings postulate the first collective cellular mechanism in the development of bicuspid aortic value as well as elucidating the link with arterial wall abnormalities and outflow misalignment defects.

• 14-3-3ε plays a role in cardiac ventricular compaction by regulating the cardiomyocyte cell cycle:14-3-3ε is an adapter protein expressed in the lateral plate mesoderm, however an in- vivo cardiac role is yet to be identified. This study demonstrates that the human 14-3-3ε protein is a vital gene in human endothelial cells and has its mRNA and protein concentrations strongly regulated. This protein plays a crucial function in cardiac development by modulating the thickness of compact myocardium formation. Deletion and mutations of 14-3-3ε, has a cardiac phenotype, with significant implications for human cardiac genetics. The findings did not demonstrate to stimulate compensation by other 14-3-3 isoforms however consequently lead to ventricular noncompaction, with distinctive features similar to Left ventricular noncompaction (LVNC)- as a outcome of a selective reduction in compact myocardium thickness. This provided evidence that 14-3-3ε is necessary for ventricular morphogenesis and controls the growth of the compact ventricular myocardium by regulating the cardiomyocyte cell cycle via both cyclin E1 and p27Kip1.

• Eomesodermin induces Mesp1 expression and cardiac differentiation from embryonic stem cells in the absence of Activin:

• Vulnerability of the developing heart to oxygen deprivation as a cause of congenital heart defects:

Historic Findings

https://www.youtube.com/watch?v=WXLPxjJszio

--Z3418340 (talk) 00:21, 27 August 2014 (EST)