Methodology for SMA Valve Development Illustrated by the Development of a SMA Pinch Valve

2015 ◽  
pp. 151-178
Author(s):  
Sven Langbein ◽  
Alexander Czechowicz
Keyword(s):  
Valve Development ◽  
Pinch Valve

scholarly journals PDGFRα: Expression and Function during Mitral Valve Morphogenesis

2021 ◽  
Vol 8 (3) ◽  
pp. 28
Author(s):  
Kelsey Moore ◽  
Diana Fulmer ◽  
Lilong Guo ◽  
Natalie Koren ◽  
Janiece Glover ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Primary Cilia ◽  
Growth Factor Receptor ◽  
Akt Phosphorylation ◽  
Valve Development ◽  
Biochemical Assays ◽  
Factor Receptor Alpha ◽  
Mesenchymal Transformation ◽  
And Function

Mitral valve prolapse (MVP) is a common form of valve disease and can lead to serious secondary complications. The recent identification of MVP causal mutations in primary cilia-related genes has prompted the investigation of cilia-mediated mechanisms of disease inception. Here, we investigate the role of platelet-derived growth factor receptor-alpha (PDGFRα), a receptor known to be present on the primary cilium, during valve development using genetically modified mice, biochemical assays, and high-resolution microscopy. While PDGFRα is expressed throughout the ciliated valve interstitium early in development, its expression becomes restricted on the valve endocardium by birth and through adulthood. Conditional ablation of Pdgfra with Nfatc1-enhancer Cre led to significantly enlarged and hypercellular anterior leaflets with disrupted endothelial adhesions, activated ERK1/2, and a dysregulated extracellular matrix. In vitro culture experiments confirmed a role in suppressing ERK1/2 activation while promoting AKT phosphorylation. These data suggest that PDGFRα functions to suppress mesenchymal transformation and disease phenotypes by stabilizing the valve endocardium through an AKT/ERK pathway.

BMDO SBIR multi-function valve development testing

1998 ◽  
Author(s):  
D. Schappell ◽  
C. Geangu ◽  
S. Grisnik
Keyword(s):  
Valve Development

Development of the inlet portion of the right ventricle in the embryonic rat heart: The basis for tricuspid valve development

1994 ◽  
Vol 239 (2) ◽  
pp. 216-223 ◽  
Author(s):  
Arnold C. G. Wenink ◽  
Bert J. Wisse ◽  
Pieter M. Groenendijk
Keyword(s):  
Right Ventricle ◽  
Tricuspid Valve ◽  
Rat Heart ◽  
Valve Development ◽  
The Right

scholarly journals Wnt signaling in heart valve development and osteogenic gene induction

2010 ◽  
Vol 338 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Christina M. Alfieri ◽  
Jonathan Cheek ◽  
Santanu Chakraborty ◽  
Katherine E. Yutzey
Keyword(s):  
Wnt Signaling ◽  
Heart Valve ◽  
Gene Induction ◽  
Valve Development ◽  
Osteogenic Gene

Multiport Sleeve Valve Development and Application

1981 ◽  
Vol 107 (1) ◽  
pp. 95-111
Author(s):  
Philip H. Burgi ◽  
Raoul E. Thibault ◽  
Edward O. Green
Keyword(s):  
Valve Development

Abstract MP235: PROX1 Contributes To Cardiac Valve Disease

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
YenChun Ho ◽  
Xin Geng ◽  
Rohan Varshney ◽  
Jang Kim ◽  
Sandeep Surbrahmanian ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Heart Valves ◽  
Cardiac Valve ◽  
Valve Disease ◽  
Matrix Composition ◽  
Cardiac Valves ◽  
Aortic Valves ◽  
Mitral Valves ◽  
Valve Development ◽  
Cardiac Valve Disease

Background: Heart valves regulate the unidirectional forward flow and prevent retrograde backflow of blood during the cardiac cycle. Cardiac valve disease (CVD) is observed in approximately 2.5% of the general population and the incidence increases to ~10% in elderly people. Patients with severe CVD require surgery and effective pharmacological treatments are currently not available. PROX1 is a transcription factor that regulates the development of lymphatic, venous, and lymphovenous valves (vascular valves). We identified that PROX1 is also expressed in a subset of valvular endothelial cells (VECs) that are located on the downstream (fibrosa) side of cardiac valves. Whether PROX1 regulates cardiac valve development and disease is not known. Method and Results: We have discovered that mice lacking Prox1 in their VECs ( Prox1 ΔVEC ) develop enlarged aortic and mitral valves in which the expression of proteoglycans is increased (control, N=10; Prox1 ΔVEC , N=9, p <0.05). Echocardiography revealed moderate to severe stenosis of aortic valves of Prox1 ΔVEC mice (control, N=5; Prox1 ΔVEC , N=9, p <0.05). PROX1 regulates the expression of the transcription factor FOXC2 in the vascular valves. Similarly, we have found that the expression of FOXC2 is downregulated in the VECs of Prox1 ΔVEC mice. Specific knockdown of FOXC2 in VECs results in the thickening of aortic valves (control, N=10; shFoxc2 ΔVEC , N=8, p <0.05). Furthermore, restoration of FOXC2 expression in VECs ( Foxc2 OE-VEC ) ameliorates the thickening of the aortic valves of Prox1 ΔVEC mice ( Prox1 ΔVEC , N=9; Foxc2 OE-VEC ; Prox1 ΔVEC , N=8, p <0.05). We have also determined that the expression of platelet-derived growth factor-B ( Pdgfb ) is increased in the valve tissue of Prox1 ΔVEC mice and in PROX1 deficient sheep mitral valve VECs (MVECs) (siCtrl , N=4; siProx1 , N=4, p <0.05). Additionally, hyperactivation of PDGF-B signaling in mice results in a phenotype that is similar to Prox1 ΔVEC mice (control , N=4; Pdgfb GOF , N=3, p <0.05). Conclusion: Together these data suggest that PROX1 maintains the extracellular matrix composition of cardiac valves by regulating the expressions of FOXC2 and PDGF-B in VECs.

scholarly journals Differential Requirement of DICER1 Activity during Development of Mitral and Tricuspid Valves

2022 ◽  
Author(s):  
Shun Yan ◽  
Yin Peng ◽  
Jin Lu ◽  
Saima Shakil ◽  
Yang Shi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Tricuspid Valve ◽  
Regulatory Mechanisms ◽  
Mitral Valve Stenosis ◽  
Sequencing Analysis ◽  
Ecm Remodeling ◽  
Mitral Valves ◽  
Valve Development ◽  
Single Cell Rna Sequencing ◽  
Cell Sources

Mitral and tricuspid valves are essential for unidirectional blood flow in the heart. They are derived from similar cell sources, and yet congenital dysplasia affecting both valves is clinically rare, suggesting the presence of differential regulatory mechanisms underlying their development. We specifically inactivated Dicer1 in the endocardium during cardiogenesis, and unexpectedly found that Dicer1-deletion caused congenital mitral valve stenosis and regurgitation, while it had no impact on other valves. We showed that hyperplastic mitral valves were caused by abnormal condensation and extracellular matrix (ECM) remodeling. Our single-cell RNA Sequencing analysis revealed impaired maturation of mesenchymal cells and abnormal expression of ECM genes in mutant mitral valves. Furthermore, expression of a set of miRNAs that target ECM genes was significantly lower in tricuspid valves compared to mitral valves, consistent with the idea that the miRNAs are differentially required for mitral and tricuspid valve development. Our study thus reveals miRNA-mediated gene regulation as a novel molecular mechanism that differentially regulates mitral and tricuspid valve development, thereby enhancing our understanding of the non-association of inborn mitral and tricuspid dysplasia observed clinically.

scholarly journals Molecular Insights into Bicuspid Aortic Valve Development and the associated aortopathy

2017 ◽  
Vol 4 (4) ◽  
pp. 478-508
Author(s):  
Nikhita Bolar ◽  
◽  
Aline Verstraeten ◽  
Lut Van Laer ◽  
Bart Loeys
Keyword(s):  
Aortic Valve ◽  
Bicuspid Aortic Valve ◽  
Valve Development

scholarly journals Prox1+ Endothelial Cells in Heart Valve Development and Homeostasis

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Anna O'Donnell ◽  
Katherine Yutzey
Keyword(s):  
Endothelial Cells ◽  
Heart Valve ◽  
Valve Development
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