Cardiovascular System Note: the Cardiovascular System Develops Early (Week-3), Enabling the Embryo to Grow Beyond the Short
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Coronary Arterial Development Is Regulated by a Dll4-Jag1-Ephrinb2 Signaling Cascade
RESEARCH ARTICLE Coronary arterial development is regulated by a Dll4-Jag1-EphrinB2 signaling cascade Stanislao Igor Travisano1,2, Vera Lucia Oliveira1,2, Bele´ n Prados1,2, Joaquim Grego-Bessa1,2, Rebeca Pin˜ eiro-Sabarı´s1,2, Vanesa Bou1,2, Manuel J Go´ mez3, Fa´ tima Sa´ nchez-Cabo3, Donal MacGrogan1,2*, Jose´ Luis de la Pompa1,2* 1Intercellular Signalling in Cardiovascular Development and Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; 2CIBER de Enfermedades Cardiovasculares, Madrid, Spain; 3Bioinformatics Unit, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain Abstract Coronaries are essential for myocardial growth and heart function. Notch is crucial for mouse embryonic angiogenesis, but its role in coronary development remains uncertain. We show Jag1, Dll4 and activated Notch1 receptor expression in sinus venosus (SV) endocardium. Endocardial Jag1 removal blocks SV capillary sprouting, while Dll4 inactivation stimulates excessive capillary growth, suggesting that ligand antagonism regulates coronary primary plexus formation. Later endothelial ligand removal, or forced expression of Dll4 or the glycosyltransferase Mfng, blocks coronary plexus remodeling, arterial differentiation, and perivascular cell maturation. Endocardial deletion of Efnb2 phenocopies the coronary arterial defects of Notch mutants. Angiogenic rescue experiments in ventricular explants, or in primary human endothelial cells, indicate that EphrinB2 is a critical effector of antagonistic Dll4 and Jag1 functions in arterial morphogenesis. Thus, coronary arterial precursors are specified in the SV prior to primary coronary plexus formation and subsequent arterial differentiation depends on a Dll4-Jag1-EphrinB2 signaling *For correspondence: [email protected] (DMG); cascade. [email protected] (JLP) Competing interests: The authors declare that no Introduction competing interests exist. -
Te2, Part Iii
TERMINOLOGIA EMBRYOLOGICA Second Edition International Embryological Terminology FIPAT The Federative International Programme for Anatomical Terminology A programme of the International Federation of Associations of Anatomists (IFAA) TE2, PART III Contents Caput V: Organogenesis Chapter 5: Organogenesis (continued) Systema respiratorium Respiratory system Systema urinarium Urinary system Systemata genitalia Genital systems Coeloma Coelom Glandulae endocrinae Endocrine glands Systema cardiovasculare Cardiovascular system Systema lymphoideum Lymphoid system Bibliographic Reference Citation: FIPAT. Terminologia Embryologica. 2nd ed. FIPAT.library.dal.ca. Federative International Programme for Anatomical Terminology, February 2017 Published pending approval by the General Assembly at the next Congress of IFAA (2019) Creative Commons License: The publication of Terminologia Embryologica is under a Creative Commons Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0) license The individual terms in this terminology are within the public domain. Statements about terms being part of this international standard terminology should use the above bibliographic reference to cite this terminology. The unaltered PDF files of this terminology may be freely copied and distributed by users. IFAA member societies are authorized to publish translations of this terminology. Authors of other works that might be considered derivative should write to the Chair of FIPAT for permission to publish a derivative work. Caput V: ORGANOGENESIS Chapter 5: ORGANOGENESIS -
Fetal Blood Flow and Genetic Mutations in Conotruncal Congenital Heart Disease
Journal of Cardiovascular Development and Disease Review Fetal Blood Flow and Genetic Mutations in Conotruncal Congenital Heart Disease Laura A. Dyer 1 and Sandra Rugonyi 2,* 1 Department of Biology, University of Portland, Portland, OR 97203, USA; [email protected] 2 Department of Biomedical Engineering, Oregon Health & Science University, Portland, OR 97239, USA * Correspondence: [email protected] Abstract: In congenital heart disease, the presence of structural defects affects blood flow in the heart and circulation. However, because the fetal circulation bypasses the lungs, fetuses with cyanotic heart defects can survive in utero but need prompt intervention to survive after birth. Tetralogy of Fallot and persistent truncus arteriosus are two of the most significant conotruncal heart defects. In both defects, blood access to the lungs is restricted or non-existent, and babies with these critical conditions need intervention right after birth. While there are known genetic mutations that lead to these critical heart defects, early perturbations in blood flow can independently lead to critical heart defects. In this paper, we start by comparing the fetal circulation with the neonatal and adult circulation, and reviewing how altered fetal blood flow can be used as a diagnostic tool to plan interventions. We then look at known factors that lead to tetralogy of Fallot and persistent truncus arteriosus: namely early perturbations in blood flow and mutations within VEGF-related pathways. The interplay between physical and genetic factors means that any one alteration can cause significant disruptions during development and underscore our need to better understand the effects of both blood flow and flow-responsive genes. -
MDCT of Interatrial Septum
Diagnostic and Interventional Imaging (2015) 96, 891—899 PICTORIAL REVIEW /Cardiovascular imaging MDCT of interatrial septum ∗ D. Yasunaga , M. Hamon Service de radiologie, pôle d’imagerie, CHU de Caen, avenue de la Côte-de-Nacre, 14033 Caen Cedex 9, France KEYWORDS Abstract ECG-gated cardiac multidetector row computed tomography (MDCT) allows precise Cardiac CT; analysis of the interatrial septum (IAS). This pictorial review provides a detailed description of Interatrial septum; the normal anatomy, variants and abnormalities of the IAS such as patent foramen ovale, con- Patent foramen genital abnormalities such as atrial septal defects as well as tumors and tumoral-like processes ovale; that develop on the IAS. Secundum ASD © 2015 Published by Elsevier Masson SAS on behalf of the Éditions françaises de radiologie. Introduction Major technical advances in computed tomography (CT) in recent years have made it pos- sible to use multidetector row CT (MDCT) in the field of cardiac imaging. Besides coronary arteries, ECG-gated cardiac MDCT provides high-resolution images of all cardiac structures. It is therefore important for radiologists to understand and be able to analyze the normal anatomical structures, variants and diseases of these different structures. This article provides an analysis of the interatrial septum (IAS) based on a pictorial review. After a short embryological and anatomical description, we will illustrate the nor- mal anatomy and variants of the IAS, anomalies such as patent foramen ovale (PFO), congenital diseases such as atrial septal defects (ASD) as well as tumors and tumoral-like processes that develop on the IAS. Abbreviations: ASA, atrial septal aneurysm; ASD, atrial septal defect; ECG, electrocardiogram; IAS, interatrial septum; IVC, inferior vena cava; IVS, interventricular septum; LV, left ventricle; M, myxoma; PFO, patent foramen ovale; RSPV, right superior pulmonary vein; RV, right ventricle; SVC, superior vena cava; MIP, maximal intensity projection; TEE, transesophageal echocardiography; TV, tricuspid valve. -
Of the Bulbus Cordis
Dr.Amjad Sahatarat 1 Two opposing ridges are developed in the walls of the Truncus Arteriosus Called Truncal ridges And in the walls of Bulbus Cordis Called Bulbar ridges The bulbus cordis is also some times named conus and therefore The ridges developed inside it are also called conal. And with those developed in the truncus arteriosus they also together called These ridges are derived mainly from the Conotruncal Ridges neural crest When these ridges are fused with each other, They form Septa So ridges developed in the truncus arteriosus ridges developed in the lumen of the bulbus after their fusion are called cordis after their fusion are called Truncal septum bulbar septum We will study first of all the bulbar septum The Distal bulbar septum The Proximal bulbar septum The proximal bulbar septum shares A) in closing the interventricular foramen The proximal bulbar septum also B) incorporated into the walls of the definitive ventricles in several ways: into the infundibulum and the vestibule In the right ventricle, the bulbus cordis is represented by the conus arteriosus (infundibulum), which gives origin to the pulmonary trunk Dr.Amjad Sahatarat 6 In the left ventricle, the bulbus cordis forms the walls of the aortic vestibule the part of the ventricular cavity just inferior to the aortic valve. The distal bulbar septum 1- Four endocardinal cushions ( one anterior, one posterior, and two lateral right and left) are developed in the distal part of the bulbus cordis. 2- A ridge is developed in the middle of each of the two lateral cushions. It should be noted that the development of these ridges will divide each of the lateral cushions into two Dr.Amjad Sahatarat 9 3-These ridges will fuse to form a complete septum called the distal bulbar septum. -
Genetic and Flow Anomalies in Congenital Heart Disease
Published online: 2021-05-10 AIMS Genetics, 3(3): 157-166. DOI: 10.3934/genet.2016.3.157 Received: 01 July 2016 Accepted: 16 August 2016 Published: 23 August 2016 http://www.aimspress.com/journal/Genetics Review Genetic and flow anomalies in congenital heart disease Sandra Rugonyi* Department of Biomedical Engineering, Oregon Health & Science University, 3303 SW Bond Ave. M/C CH13B, Portland, OR 97239, USA * Correspondence: Email: [email protected]; Tel: +1-503-418-9310; Fax: +1-503-418-9311. Abstract: Congenital heart defects are the most common malformations in humans, affecting approximately 1% of newborn babies. While genetic causes of congenital heart disease have been studied, only less than 20% of human cases are clearly linked to genetic anomalies. The cause for the majority of the cases remains unknown. Heart formation is a finely orchestrated developmental process and slight disruptions of it can lead to severe malformations. Dysregulation of developmental processes leading to heart malformations are caused by genetic anomalies but also environmental factors including blood flow. Intra-cardiac blood flow dynamics plays a significant role regulating heart development and perturbations of blood flow lead to congenital heart defects in animal models. Defects that result from hemodynamic alterations recapitulate those observed in human babies, even those due to genetic anomalies and toxic teratogen exposure. Because important cardiac developmental events, such as valve formation and septation, occur under blood flow conditions while the heart is pumping, blood flow regulation of cardiac formation might be a critical factor determining cardiac phenotype. The contribution of flow to cardiac phenotype, however, is frequently ignored. -
Extensive Vasculogenesis, Angiogenesis, and Organogenesis Precede Lethality in Mice Lacking All V Integrins
Cell, Vol. 95, 507–519, November 13, 1998, Copyright ©1998 by Cell Press Extensive Vasculogenesis, Angiogenesis, and Organogenesis Precede Lethality in Mice Lacking All ␣v Integrins Bernhard L. Bader,*‡ Helen Rayburn,* their ligands. Significant expression of ␣v integrins has Denise Crowley,* and Richard O. Hynes*† been noted, in particular, in neural crest cells (Delannet * Howard Hughes Medical Institute et al., 1994), glial cells (Hirsch et al., 1994; Milner and Center for Cancer Research ffrench-Constant, 1994), muscle (Hirsch et al., 1994; Mc- and Department of Biology Donald et al., 1995; Martin and Sanes, 1997), osteoclasts Massachusetts Institute of Technology (Va¨ a¨ na¨ nen and Horton, 1995), epithelia (␣v6; Breuss et Cambridge, Massachusetts 02139 al., 1995; Huang et al., 1996), and blood vessels during development (Brooks et al., 1994a; Drake et al., 1995; Friedlander et al., 1995, 1996) or angiogenesis in re- Summary sponse to tumors (Brooks et al., 1994a, 1994b, 1996, 1998; Varner et al., 1995). ␣v integrins have been implicated in many develop- Among the ligands for various ␣v integrins is fibro- mental processes and are therapeutic targets for inhi- nectin (FN), and results on mouse embryos lacking FN bition of angiogenesis and osteoporosis. Surprisingly, or FN receptor integrins suggest that ␣v integrins might ablation of the gene for the ␣v integrin subunit, elimi- be important receptors for FN during early development. nating all five ␣v integrins, although causing lethality, FN-null embryos fail to form notochord or somites allows considerable development and organogenesis (George et al., 1993; Georges-Labouesse et al., 1996), including, most notably, extensive vasculogenesis and whereas embryos null for either (Yang et al., 1993, 1995) angiogenesis. -
The Evolving Cardiac Lymphatic Vasculature in Development, Repair and Regeneration
REVIEWS The evolving cardiac lymphatic vasculature in development, repair and regeneration Konstantinos Klaourakis 1,2, Joaquim M. Vieira 1,2,3 ✉ and Paul R. Riley 1,2,3 ✉ Abstract | The lymphatic vasculature has an essential role in maintaining normal fluid balance in tissues and modulating the inflammatory response to injury or pathogens. Disruption of normal development or function of lymphatic vessels can have severe consequences. In the heart, reduced lymphatic function can lead to myocardial oedema and persistent inflammation. Macrophages, which are phagocytic cells of the innate immune system, contribute to cardiac development and to fibrotic repair and regeneration of cardiac tissue after myocardial infarction. In this Review, we discuss the cardiac lymphatic vasculature with a focus on developments over the past 5 years arising from the study of mammalian and zebrafish model organisms. In addition, we examine the interplay between the cardiac lymphatics and macrophages during fibrotic repair and regeneration after myocardial infarction. Finally, we discuss the therapeutic potential of targeting the cardiac lymphatic network to regulate immune cell content and alleviate inflammation in patients with ischaemic heart disease. The circulatory system of vertebrates is composed of two after MI. In this Review, we summarize the current complementary vasculatures, the blood and lymphatic knowledge on the development, structure and function vascular systems1. The blood vasculature is a closed sys- of the cardiac lymphatic vasculature, with an emphasis tem responsible for transporting gases, fluids, nutrients, on breakthroughs over the past 5 years in the study of metabolites and cells to the tissues2. This extravasation of cardiac lymphatic heterogeneity in mice and zebrafish. -
Tetralogy of Fallot with Pulmonary Obstruction at the Level of the Conus Inlet a CASE REPORT
6 April 1974 S.-A. MEDIESE TYDSKRIF 677 Tetralogy of Fallot with Pulmonary Obstruction at the Level of the Conus Inlet A CASE REPORT T. MULLER SUMMARY in diameter could be seen. The right ventricle was enlarged and the thickness of the wall was 13,5 mm, compared with A case of Fallot's tetralogy is described in a Black male the 12,5 mm thickness of the left ventricle. The right who died of acute cardiac failure at the age of 17 years. ventricle communicated with the left ventricle through a The conus arteriosus was practically a separate chamber very large defect of the interventricular septum, which communicating with the right ventricle through a very easily admitted 3 fingers and which was straddled by the small ostium. The embryology of the truncus arteriosus aorta. The right ventricle was completely demarcated from the bulbus cordis is discussed in the light of the anomalies the infundibulum or conus arteriosus, the only connection described here. The question of maintenance of the pul being an ostium of 7,5 mm in diameter. monary circulation in the absence of an open ductus The conus arteriosus was a well-developed entity, both arteriosus is discussed. externally and internally (Figs 1 and 2). The interior of the conus arteriosus adjoining the right ventricle showed trabeculae carneae, but the upper portion leading to the S. Air. Med. J.• 48, 677 (1974). pulmonary valve was smooth. The pulmonary artery was reduced in size to half of that of the aort'i, and had only 2 valves (Fig. 2). -
EXTRACORONARY CARDIAC VEINS in the RAT1 the Present Work
EXTRACORONARY CARDIAC VEINS IN THE RAT1 MYRON H. HALPERN Department of Anatomy, Unit-ersity of Michigan, Ann Arbor SIX FIGURES The present work had its inception in the discovery of vessels around the rat’s heart which did not correspond to anything previously described in other mammals. These ves- sels are a system of veins which begin on the heart and terminate in the anterior venae cavae. Two major veins eom- prise this system, each of which crosses the midline to empty into the contralateral anterior vena cava. They drain the conal region of the right ventricle and the ventrocephalic region of the left ventricle. The term “extracoronary” cardiac veins has been applied to these vessels by the author because they originate on the heart and terminate in remote vessels not otherwise associated with the coronary circulation. Al- though this system has been found to exist in certain fishes and amphibians, to the author’s knowledge it has never been recognized in mammals. These findings seemed to warrant a more detailed study of the adult cardiac venous drainage of the rat. To supplement this portion of the investigation, an embryologic study was undertaken. Both the adult and the embryonic patterns of the cardiac drainage were com- pared with the patterns found in the above vertebrates and were interpreted on the basis of these comparisons. MATERIAL AND METHODS For this study, the venous system of 85 adult rats were injected with latex preparatory to dissection. Of this number, Portion of a dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the University of Michigan. -
Development of HEART 4-VEINS
Development of brachiocephalic veins 1. Right brachiocephalic vein is formed by cranial part of right anterior cardinal vein and 2. Left brachiocephalic is formed by cranial part of left anterior cardinal vein and the interant.cardinal anastomosis. Development of superior vena cava 1. The part up to the opening of vena azygos develops from caudal part of right ant.cardinal vein and 2. The part below the opening (intrapericardial part) is formed by the right common cardinal vein. Development of azygos and hemiazygos veins A. 1. Vena azygos develops from right azygos line vein and 2. The arch of vena azygos is formed by the cranial end of right postcardinal vein. B. Hemiazygos veins are formed by the left azygos line vein. Development of Inferior vena cava Inferior vena cava is formed, from below upwards by: 1. Begins by the union of the two common iliac veins (postcardinal veins), 2. Right supracardinal, 3. Right supra-subcardinal anastomosis, 4. Right subcardinal, 5. New formation (hepatic segment) and 6. Hepatocardiac channel (terminal part of right vitelline vein). Congenital anomalies • Double inferior vena cava • Absence • Left SVC • Double SVC DEVELOPMENT OF PORTAL VEIN 1. The portal vein is formed behind the neck of pancreas by the union of superior mesentric and splenic vein to the left vitelline vein. 2. The part of the portal vein which is behind the Ist part of duodenum is formed by middle dorsal transverse anastomosis. 3. Part of portal vein which is in the free margin of lesser omentum is formed by cranial or distal part of right vitelline vein. -
Azygos Vein System Abnormality: Case Report
Gülhane Týp Dergisi 2006; 48: 180-182 OLGU SUNUMU © Gülhane Askeri Týp Akademisi 2006 Azygos vein system abnormality: case report Necdet Kocabýyýk (*), Tunç Kutoðlu (**), Soner Albay (*), Bülent Yalçýn (*), Hasan Ozan (*) Summary Introduction Variations seen in the thoracic vein system are Abnormalities related to the azygos system are not rare (1). In a series related to the development of these veins. of 200 cases, Bergman et al. have reported the incidence of this anomaly During the dissection from the posterior medi- astinum of the 60-year-old male cadaver, it 26% (2). These abnormalities are generally explained by the embryolog- was observed that there was no complete ical development. Venous branching of the azygos vein varies (3). There accessory hemiazygos vein, and both posterior are two origins of the azygos and hemiazygos veins. By union of these intercostal veins and hemiazygos vein (above origins and regression of some parts, azygos system comes into its final T10 level) drained bilaterally to the azygos vein. Considering these types of variations is status (4). Different types of structures may occur when these veins important during imaging this region and surgi- develop. Abnormalities about azygos system and especially the variations cal operations. of the hemiazygos veins are not clearly described in the literature. In this Key words: Azygos vein, hemiazygos vein, superior vena cava, venous anomaly presentation absence of the accessory hemiazygos vein and possible causes of these types of variations are discussed in view of the embry- Özet ological development. Azigos ven sistem anomalisi: olgu sunumu Toraks ven sisteminde görülen varyasyonlar, embriyolojik olarak bu venlerin geliþimiyle ilgi- Case Report lidir.