Difference between revisions of "Talk:Cardiovascular System Development"

From Embryology
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==2010==
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===An endocardial pathway involving Tbx5, Gata4, and Nos3 required for atrial septum formation===
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Proc Natl Acad Sci U S A. 2010 Oct 25. [Epub ahead of print]
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Nadeau M, Georges RO, Laforest B, Yamak A, Lefebvre C, Beauregard J, Paradis P, Bruneau BG, Andelfinger G, Nemer M.
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Research Unit in Cardiac Growth and Differentiation and Molecular Biology Program, Université de Montréal, Montréal, QC, Canada H3C 3J7.
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Abstract
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In humans, septal defects are among the most prevalent congenital heart diseases, but their cellular and molecular origins are not fully understood. We report that transcription factor Tbx5 is present in a subpopulation of endocardial cells and that its deletion therein results in fully penetrant, dose-dependent atrial septal defects in mice. Increased apoptosis of endocardial cells lacking Tbx5, as well as neighboring TBX5-positive myocardial cells of the atrial septum through activation of endocardial NOS (Nos3), is the underlying mechanism of disease. Compound Tbx5 and Nos3 haploinsufficiency in mice worsens the cardiac phenotype. The data identify a pathway for endocardial cell survival and unravel a cell-autonomous role for Tbx5 therein. The finding that Nos3, a gene regulated by many congenital heart disease risk factors including stress and diabetes, interacts genetically with Tbx5 provides a molecular framework to understand gene-environment interaction in the setting of human birth defects.
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PMID: 20974940
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http://www.ncbi.nlm.nih.gov/pubmed/20974940
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http://www.pnas.org/content/107/45/19356.full
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==Heart Valve Development==
 
==Heart Valve Development==
  
Transcriptional Regulation of Heart Valve Progenitor Cells
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===Transcriptional Regulation of Heart Valve Progenitor Cells===
 
PEDIATRIC CARDIOLOGY
 
PEDIATRIC CARDIOLOGY
 
Volume 31, Number 3, 414-421, DOI: 10.1007/s00246-009-9616-x
 
Volume 31, Number 3, 414-421, DOI: 10.1007/s00246-009-9616-x
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http://onlinelibrary.wiley.com/doi/10.1002/dvdy.22458/full
 
http://onlinelibrary.wiley.com/doi/10.1002/dvdy.22458/full
  
Wnt signaling in heart valve development and osteogenic gene induction.
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===Wnt signaling in heart valve development and osteogenic gene induction===
 
Alfieri CM, Cheek J, Chakraborty S, Yutzey KE.
 
Alfieri CM, Cheek J, Chakraborty S, Yutzey KE.
 
Dev Biol. 2010 Feb 15;338(2):127-35. Epub 2009 Dec 1.
 
Dev Biol. 2010 Feb 15;338(2):127-35. Epub 2009 Dec 1.

Revision as of 07:17, 10 November 2010

2010

An endocardial pathway involving Tbx5, Gata4, and Nos3 required for atrial septum formation

Proc Natl Acad Sci U S A. 2010 Oct 25. [Epub ahead of print]

Nadeau M, Georges RO, Laforest B, Yamak A, Lefebvre C, Beauregard J, Paradis P, Bruneau BG, Andelfinger G, Nemer M.

Research Unit in Cardiac Growth and Differentiation and Molecular Biology Program, Université de Montréal, Montréal, QC, Canada H3C 3J7.

Abstract In humans, septal defects are among the most prevalent congenital heart diseases, but their cellular and molecular origins are not fully understood. We report that transcription factor Tbx5 is present in a subpopulation of endocardial cells and that its deletion therein results in fully penetrant, dose-dependent atrial septal defects in mice. Increased apoptosis of endocardial cells lacking Tbx5, as well as neighboring TBX5-positive myocardial cells of the atrial septum through activation of endocardial NOS (Nos3), is the underlying mechanism of disease. Compound Tbx5 and Nos3 haploinsufficiency in mice worsens the cardiac phenotype. The data identify a pathway for endocardial cell survival and unravel a cell-autonomous role for Tbx5 therein. The finding that Nos3, a gene regulated by many congenital heart disease risk factors including stress and diabetes, interacts genetically with Tbx5 provides a molecular framework to understand gene-environment interaction in the setting of human birth defects.

PMID: 20974940 http://www.ncbi.nlm.nih.gov/pubmed/20974940

http://www.pnas.org/content/107/45/19356.full


Heart Valve Development

Transcriptional Regulation of Heart Valve Progenitor Cells

PEDIATRIC CARDIOLOGY Volume 31, Number 3, 414-421, DOI: 10.1007/s00246-009-9616-x

"The development and normal function of the heart valves requires complex interactions among signaling molecules, transcription factors and structural proteins that are tightly regulated in time and space. Here we review the roles of critical transcription factors that are required for specific aspects of normal valve development. The early progenitors of the heart valves are localized in endocardial cushions that express transcription factors characteristic of mesenchyme, including Twist1, Tbx20, Msx1 and Msx2. As the valve leaflets mature, they are composed of complex stratified extracellular matrix proteins that are regulated by the transcriptional functions of NFATc1, Sox9, and Scleraxis. Each of these factors has analogous functions in differentiation of related connective tissue lineages. Together, the precise timing and localized functions of specific transcription factors control cell proliferation, differentiation, elongation, and remodeling processes that are necessary for normal valve structure and function. In addition, there is increasing evidence that these same transcription factors contribute to congenital, as well as degenerative, valve disease."

Regulation of heart valve morphogenesis by Eph receptor ligand, ephrin-A1

http://onlinelibrary.wiley.com/doi/10.1002/dvdy.22458/full

Wnt signaling in heart valve development and osteogenic gene induction

Alfieri CM, Cheek J, Chakraborty S, Yutzey KE. Dev Biol. 2010 Feb 15;338(2):127-35. Epub 2009 Dec 1. PMID: 19961844

Heart valve development: regulatory networks in development and disease. Combs MD, Yutzey KE. Circ Res. 2009 Aug 28;105(5):408-21. Review. PMID: 19713546


A new role for the human placenta as a hematopoietic site throughout gestation.

http://www.ncbi.nlm.nih.gov/pubmed/19208786

We investigated whether the human placenta contributes to embryonic and fetal hematopoietic development. Two cell populations--CD34(++)CD45(low) and CD34( +)CD45(low)--were found in chorionic villi. CD34(++) CD45(low) cells display many markers that are characteristic of multipotent primitive hematopoietic progenitors and hematopoietic stem cells. Clonogenic in vitro assays showed that CD34(++)CD45( low) cells contained colony-forming units-culture with myeloid and erythroid potential and differentiated into CD56(+) natural killer cells and CD19(+) B cells in culture. CD34(+)CD45(low) cells were mostly enriched in erythroid- and myeloid-committed progenitors. While the number of CD34(++)CD45(low) cells increased throughout gestation in parallel with placental mass. However, their density (cells per gram of tissue) reached its peak at 5 to 8 weeks, decreasing more than 7-fold from the ninth week onward. In addition to multipotent progenitors, the placenta contained intermediate progenitors, indicative of active hematopoiesis. Together, these data suggest that the human placenta is potentially an important hematopoietic organ, opening the possibility of banking placental hematopoietic stem cells along with cord blood for transplantation.


  • Endothelial cell lineages of the heart. Ishii Y, Langberg J, Rosborough K, Mikawa T. Cell Tissue Res. 2009 Jan;335(1):67-73. Epub 2008 Aug 6. Review. PMID: 18682987 | PMC: 2729171

The links in this next sections are to the original 2008 online notes pages for Cardiovascular System Development.

Cardiovascular Notes Introduction | Abnormalities | Stage 13/14 | Stage 22 | Stage 22 Selected Highpower | Heart | Heart Rate | BloodBlood Vessels | Molecular | Lymphatic | Text only page | WWW Links | Postnatal | History - Harvey

Cardiovascular Movies Heart Movies | Heart Looping | Atrial Septation | Realignment | Ventricular Septation | Heart Septation Models | Historic Heart Movie |

Other Cardiac and Vascular Movies Fetal Circulation (Before Birth) | Circulation (After Birth) | Aortic Branches to Glands (Kidneys only) | Aortic Branches to Glands (Gonads only)


Coronary Vessels

  • Origin, fate, and function of epicardium-derived cells (EPDCs) in normal and abnormal cardiac development.[1] Lie-Venema H, van den Akker NM, Bax NA, Winter EM, Maas S, Kekarainen T, Hoeben RC, deRuiter MC, Poelmann RE, Gittenberger-de Groot AC. ScientificWorldJournal. 2007 Nov 12;7:1777-98. Review. PMID: 18040540 | PDF full article
  • Cellular and molecular mechanisms of coronary vessel development.[2] Mu H, Ohashi R, Lin P, Yao Q, Chen C. Vasc Med. 2005 Feb;10(1):37-44. Review. PMID: 15920999


http://www.mediawiki.org/wiki/Extension:Pubmed


  • Development of innervation of coronary arteries in human foetus up until 230 mm. stage (mid-term). Br Heart J. 1970 Jan;32(1):108-13.

Smith RB.

PMID: 5417838

  • Innervation of the coronary vessels is initiated before the 30mm. stage of development.
  • All the main branches of the coronary arteries are formed and in their definitive positions by the 40 mm. stage.
  • Two plexuses have been shown for all the larger vessels after the 120 mm. stage.
  • There are coarse-fibre and fine-fibre plexuses, situated at different levels in the tunica adventitia.
  • Ganglion cells have been found in relation to the coronary arteries over the ventricles.
  • This confirms the part played by the vagal system in the innervation of the ventricle.
  • No nerve endings were seen in the tunica media.

References

  1. <pubmed>18040540</pubmed>
  2. <pubmed>15920999</pubmed>