scholarly journals A spatiotemporal evaluation of the contribution of the dorsal mesenchymal protrusion to cardiac development

2007 ◽  
Vol 236 (5) ◽  
pp. spc1-spc1
Author(s):  
Brian S. Snarr ◽  
Elaine E. Wirrig ◽  
Aimee L. Phelps ◽  
Thomas C. Trusk ◽  
Andy Wessels
Keyword(s):  
Cardiac Development ◽  
Dorsal Mesenchymal Protrusion

scholarly journals A spatiotemporal evaluation of the contribution of the dorsal mesenchymal protrusion to cardiac development

2007 ◽  
Vol 236 (5) ◽  
pp. 1287-1294 ◽  
Author(s):  
Brian S. Snarr ◽  
Elaine E. Wirrig ◽  
Aimee L. Phelps ◽  
Thomas C. Trusk ◽  
Andy Wessels
Keyword(s):  
Cardiac Development ◽  
Dorsal Mesenchymal Protrusion

Angiotensin2-receptors in postnatal cardiac development

2009 ◽  
Vol 56 (S 01) ◽  
Author(s):  
D Biermann ◽  
L Conradi ◽  
H Treede ◽  
A Heimann ◽  
M Didié ◽  
...  
Keyword(s):  
Cardiac Development

scholarly journals Recapitulating Cardiac Structure and Function In Vitro from Simple to Complex Engineering

Micromachines ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 386
Author(s):  
Ana Santos ◽  
Yongjun Jang ◽  
Inwoo Son ◽  
Jongseong Kim ◽  
Yongdoo Park
Keyword(s):  
Tissue Engineering ◽  
Extracellular Matrix ◽  
Computational Modeling ◽  
Cardiac Tissue ◽  
Cardiac Development ◽  
Heart Tissue ◽  
Cardiac Tissue Engineering ◽  
Cardiac Cells

Cardiac tissue engineering aims to generate in vivo-like functional tissue for the study of cardiac development, homeostasis, and regeneration. Since the heart is composed of various types of cells and extracellular matrix with a specific microenvironment, the fabrication of cardiac tissue in vitro requires integrating technologies of cardiac cells, biomaterials, fabrication, and computational modeling to model the complexity of heart tissue. Here, we review the recent progress of engineering techniques from simple to complex for fabricating matured cardiac tissue in vitro. Advancements in cardiomyocytes, extracellular matrix, geometry, and computational modeling will be discussed based on a technology perspective and their use for preparation of functional cardiac tissue. Since the heart is a very complex system at multiscale levels, an understanding of each technique and their interactions would be highly beneficial to the development of a fully functional heart in cardiac tissue engineering.

scholarly journals Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes

2021 ◽  
Vol 22 (7) ◽  
pp. 3616
Author(s):  
Ewelina Jozefczuk ◽  
Piotr Szczepaniak ◽  
Tomasz Jan Guzik ◽  
Mateusz Siedlinski
Keyword(s):  
Cardiac Development ◽  
Glycogen Synthase ◽  
Sphingosine Kinase ◽  
Negative Control ◽  
Neonatal Mouse ◽  
Sphingosine Kinase 1 ◽  
Postnatal Maturation ◽  
Neonatal Cardiomyocytes ◽  
Pathological Cardiac Hypertrophy

Sphingosine kinase-1 (Sphk1) and its product, sphingosine-1-phosphate (S1P) are important regulators of cardiac growth and function. Numerous studies have reported that Sphk1/S1P signaling is essential for embryonic cardiac development and promotes pathological cardiac hypertrophy in adulthood. However, no studies have addressed the role of Sphk1 in postnatal cardiomyocyte (CM) development so far. The present study aimed to assess the molecular mechanism(s) by which Sphk1 silencing might influence CMs development and hypertrophy in vitro. Neonatal mouse CMs were transfected with siRNA against Sphk1 or negative control, and subsequently treated with 1 µM angiotensin II (AngII) or a control buffer for 24 h. The results of RNASeq analysis revealed that diminished expression of Sphk1 significantly accelerated neonatal CM maturation by inhibiting cell proliferation and inducing developmental pathways in the stress (AngII-induced) conditions. Importantly, similar effects were observed in the control conditions. Enhanced maturation of Sphk1-lacking CMs was further confirmed by the upregulation of the physiological hypertrophy-related signaling pathway involving Akt and downstream glycogen synthase kinase 3 beta (Gsk3β) downregulation. In summary, we demonstrated that the Sphk1 silencing in neonatal mouse CMs facilitated their postnatal maturation in both physiological and stress conditions.

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