scholarly journals Cardiac function modulates endocardial cell dynamics to shape the cardiac outflow tract

2019 ◽  
Author(s):  
Pragya Sidhwani ◽  
Giulia L.M. Boezio ◽  
Hongbo Yang ◽  
Neil C. Chi ◽  
Beth L. Roman ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Outflow Tract ◽  
Cell Dynamics ◽  
Cell Behaviors ◽  
Cell Accumulation ◽  
Tgfβ Receptor ◽  
Heart Formation ◽  
Physical Forces ◽  
Endocardial Cell ◽  
Cardiac Outflow

ABSTRACTPhysical forces are important participants in the cellular dynamics that shape developing organs. During heart formation, for example, contractility and blood flow generate biomechanical cues that influence patterns of cell behavior. Here, we address the interplay between function and form during the assembly of the cardiac outflow tract (OFT), a crucial connection between the heart and vasculature that develops while circulation is underway. In zebrafish, we find that the OFT expands via accrual of both endocardial and myocardial cells. However, when cardiac function is disrupted, OFT endocardial growth ceases, accompanied by reduced proliferation and reduced addition of cells from adjacent vessels. The TGFβ receptor Acvrl1 is required for addition of endocardial cells, but not for their proliferation, indicating distinct regulation of these essential cell behaviors. Together, our results suggest that cardiac function modulates OFT morphogenesis by triggering endocardial cell accumulation that induces OFT lumen expansion and shapes OFT dimensions.

scholarly journals Cardiac function modulates endocardial cell dynamics to shape the cardiac outflow tract

Development ◽  
2020 ◽  
Vol 147 (12) ◽  
pp. dev185900
Author(s):  
Pragya Sidhwani ◽  
Dena M. Leerberg ◽  
Giulia L. M. Boezio ◽  
Teresa L. Capasso ◽  
Hongbo Yang ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Outflow Tract ◽  
Cell Dynamics ◽  
Endocardial Cell ◽  
Cardiac Outflow

Expression of the chick Sizzled gene in progenitors of the cardiac outflow tract

2008 ◽  
Vol 8 (6) ◽  
pp. 471-476 ◽  
Author(s):  
Lars Wittler ◽  
Michael Saborowski ◽  
Michael Kessel
Keyword(s):  
Outflow Tract ◽  
Cardiac Outflow

scholarly journals Endocardial cell epithelial-mesenchymal transformation requires Type III TGFβ receptor interaction with GIPC

2012 ◽  
Vol 24 (1) ◽  
pp. 247-256 ◽  
Author(s):  
Todd A. Townsend ◽  
Jamille Y. Robinson ◽  
Tam How ◽  
Daniel M. DeLaughter ◽  
Gerard C. Blobe ◽  
...  
Keyword(s):  
Receptor Interaction ◽  
Type Iii ◽  
Tgfβ Receptor ◽  
Endocardial Cell ◽  
Mesenchymal Transformation

Defects in cardiac outflow tract formation and pro-B-lymphocyte expansion in mice lacking Sox-4

Nature ◽  
1996 ◽  
Vol 380 (6576) ◽  
pp. 711-714 ◽  
Author(s):  
Marco W. Schilham ◽  
Mariëtte A. Oosterwegel ◽  
Petra Moerer ◽  
Jing Ya ◽  
Piet A. J. de Boer ◽  
...  
Keyword(s):  
B Lymphocyte ◽  
Outflow Tract ◽  
Cardiac Outflow

scholarly journals 3D Tissue elongation via ECM stiffness-cued junctional remodeling

2018 ◽  
Author(s):  
Dong-Yuan Chen ◽  
Justin Crest ◽  
Sebastian J. Streichan ◽  
David Bilder
Keyword(s):  
Basement Membrane ◽  
Cell Shape ◽  
Cell Dynamics ◽  
Src Tyrosine Kinase ◽  
Average Cell ◽  
Cellular Behavior ◽  
Cell Behaviors ◽  
Oriented Cell Division ◽  
Morphometric Analyses ◽  
Membrane Stiffness

ABSTRACTOrgans are sculpted by extracellular as well as cell-intrinsic forces, but how collective cell dynamics are orchestrated in response to microenvironmental cues is poorly understood. Here we apply advanced image analysis to reveal ECM-responsive cell behaviors that drive elongation of the Drosophila follicle, a model 3D system in which basement membrane stiffness instructs tissue morphogenesis. Through in toto morphometric analyses of WT and ‘round egg’ mutants, we find that neither changes in average cell shape nor oriented cell division are required for appropriate organ shape. Instead, a major element is a reorientation of elongated cells at the follicle anterior. Polarized reorientation is regulated by mechanical cues from the basement membrane, which are transduced by the Src tyrosine kinase to alter junctional E-cadherin trafficking. This mechanosensitive cellular behavior represents a conserved mechanism that can elongate ‘edgeless’ tubular epithelia in a process distinct from those that elongate bounded, planar epithelia.

scholarly journals Prickle1mutation causes planar cell polarity and directional cell migration defects associated with cardiac outflow tract anomalies and other structural birth defects

Biology Open ◽  
2016 ◽  
Vol 5 (3) ◽  
pp. 323-335 ◽  
Author(s):  
Brian C. Gibbs ◽  
Rama Rao Damerla ◽  
Eszter K. Vladar ◽  
Bishwanath Chatterjee ◽  
Yong Wan ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Birth Defects ◽  
Planar Cell Polarity ◽  
Outflow Tract ◽  
Directional Cell Migration ◽  
Cardiac Outflow

Pax3 is required for cardiac neural crest migration in the mouse: evidence from the splotch (Sp2H) mutant

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 505-514 ◽  
Author(s):  
S.J. Conway ◽  
D.J. Henderson ◽  
A.J. Copp
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Outflow Tract ◽  
Avian Embryo ◽  
Cardiac Neural Crest ◽  
Branchial Arches ◽  
Aortic Arches ◽  
Cardiac Outflow

Neural crest cells originating in the occipital region of the avian embryo are known to play a vital role in formation of the septum of the cardiac outflow tract and to contribute cells to the aortic arches, thymus, thyroid and parathyroids. This ‘cardiac’ neural crest sub-population is assumed to exist in mammals, but without direct evidence. In this paper we demonstrate, using RT-PCR and in situ hybridisation, that Pax3 expression can serve as a marker of cardiac neural crest cells in the mouse embryo. Cells of this lineage were traced from the occipital neural tube, via branchial arches 3, 4 and 6, into the aortic sac and aorto-pulmonary outflow tract. Confirmation that these Pax3-positive cells are indeed cardiac neural crest is provided by experiments in which hearts were deprived of a source of colonising neural crest, by organ culture in vitro, with consequent lack of up-regulation of Pax3. Occipital neural crest cell outgrowths in vitro were also shown to express Pax3. Mutation of Pax3, as occurs in the splotch (Sp2H) mouse, results in development of conotruncal heart defects including persistent truncus arteriosus. Homozygotes also exhibit defects of the aortic arches, thymus, thyroid and parathyroids. Pax3-positive neural crest cells were found to emigrate from the occipital neural tube of Sp2H/Sp2H embryos in a relatively normal fashion, but there was a marked deficiency or absence of neural crest cells traversing branchial arches 3, 4 and 6, and entering the cardiac outflow tract. This decreased expression of Pax3 in Sp2H/Sp2H embryos was not due to down-regulation of Pax3 in neural crest cells, as use of independent neural crest markers, Hoxa-3, CrabpI, Prx1, Prx2 and c-met also revealed a deficiency of migrating cardiac neural crest cells in homozygous embryos. This work demonstrates the essential role of the cardiac neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that Pax3 function is required for the cardiac neural crest to complete its migration to the developing heart.

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