Relevant bibliographies by topics / Valvular interstitial cells

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Valvular interstitial cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 23 November 2024

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Journal articles on the topic "Valvular interstitial cells"

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Hjortnaes, Jesper, Kayle Shapero, Claudia Goettsch, Joshua D. Hutcheson, Joshua Keegan, Jolanda Kluin, John E. Mayer, Joyce Bischoff, and Elena Aikawa. "Valvular interstitial cells suppress calcification of valvular endothelial cells." Atherosclerosis 242, no. 1 (September 2015): 251–60. http://dx.doi.org/10.1016/j.atherosclerosis.2015.07.008.

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Bakhaty, Ahmed A., Sanjay Govindjee, and Mohammad R. K. Mofrad. "A Coupled Multiscale Approach to Modeling Aortic Valve Mechanics in Health and Disease." Applied Sciences 11, no. 18 (September 8, 2021): 8332. http://dx.doi.org/10.3390/app11188332.

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Mechano-biological processes in the aortic valve span multiple length scales ranging from the molecular and cell to tissue and organ levels. The valvular interstitial cells residing within the valve cusps sense and actively respond to leaflet tissue deformations caused by the valve opening and closing during the cardiac cycle. Abnormalities in these biomechanical processes are believed to impact the matrix-maintenance function of the valvular interstitial cells, thereby initiating valvular disease processes such as calcific aortic stenosis. Understanding the mechanical behavior of valvular interstitial cells in maintaining tissue homeostasis in response to leaflet tissue deformation is therefore key to understanding the function of the aortic valve in health and disease. In this study, we applied a multiscale computational homogenization technique (also known as “FE2”) to aortic valve leaflet tissue to study the three-dimensional mechanical behavior of the valvular interstitial cells in response to organ-scale mechanical loading. We further considered calcific aortic stenosis with the aim of understanding the likely relationship between the valvular interstitial cell deformations and calcification. We find that the presence of calcified nodules leads to an increased strain profile that drives further growth of calcification.
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Gabriel, Matthias, Christian Bollensdorff, and Christophe Michel Raynaud. "Surface Modification of Polytetrafluoroethylene and Polycaprolactone Promoting Cell-Selective Adhesion and Growth of Valvular Interstitial Cells." Journal of Functional Biomaterials 13, no. 2 (June 1, 2022): 70. http://dx.doi.org/10.3390/jfb13020070.

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Tissue engineering concepts, which are concerned with the attachment and growth of specific cell types, frequently employ immobilized ligands that interact preferentially with cell types of interest. Creating multicellular grafts such as heart valves calls for scaffolds with spatial control over the different cells involved. Cardiac heart valves are mainly constituted out of two cell types, endothelial cells and valvular interstitial cells. To have control over where which cell type can be attracted would enable targeted cell settlement and growth contributing to the first step of an engineered construct. For endothelial cells, constituting the outer lining of the valve tissue, several specific peptide ligands have been described. Valvular interstitial cells, representing the bulk of the leaflet, have not been investigated in this regard. Two receptors, the integrin α9β1 and CD44, are known to be highly expressed on valvular interstitial cells. Here, we demonstrate that by covalently grafting the corresponding peptide and polysaccharide ligand onto an erodible, polycaprolactone (PCL), and a non-degradable, polytetrafluoroethylene (PTFE), polymer, surfaces were generated that strongly support valvular interstitial cell colonization with minimal endothelial cell and reduced platelet adhesion. The technology for covalent binding of corresponding ligands is a key element towards tissue engineered cardiac valves for in vitro applications, but also towards future in vivo application, especially in combination with degradable scaffold material.
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Kostyunin, A. E. "Molecular aspects of the pathological activation and differentiation of valvular interstitial cells during the development of calcific aortic stenosis." Siberian Medical Journal 34, no. 3 (November 4, 2019): 66–72. http://dx.doi.org/10.29001/2073-8552-2019-34-3-66-72.

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Calcific aortic stenosis is the most common valvular heart disease. The pathogenesis of this disease is complex and resembles the atherosclerotic process in the blood vessels. It is known that valvular interstitial cell activation and subsequent differentiation into osteoblast- and myofibroblast-like cells is the main driving force of fibrous and calcified aortic valve tissue. However, the molecular mechanisms behind these processes are still not fully understood. Current information on this issue is collected and analyzed in this article. The main molecular pathways mediating the pathological differentiation of the valvular interstitial cells and the reasons for their activation are considered.
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Jenke, Alexander, Julia Kistner, Sarah Saradar, Agunda Chekhoeva, Mariam Yazdanyar, Ann Kathrin Bergmann, Melanie Vera Rötepohl, Artur Lichtenberg, and Payam Akhyari. "Transforming growth factor-β1 promotes fibrosis but attenuates calcification of valvular tissue applied as a three-dimensional calcific aortic valve disease model." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 5 (November 1, 2020): H1123—H1141. http://dx.doi.org/10.1152/ajpheart.00651.2019.

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Employing aortic valve leaflets as a tissue-based three-dimensional disease model, our study investigates the role of transforming growth factor (TGF)-β1 in calcific aortic valve disease pathogenesis. We find that, by activating Mothers against decapentaplegic homolog 3, TGF-β1 intensifies expressional and proliferative activation along with myofibroblastic differentiation of valvular interstitial cells, thus triggering dominant fibrosis. Simultaneously, by inhibiting activation of Mothers against decapentaplegic homolog 1/5/8 and canonical Wnt/β-catenin signaling, TGF-β1 attenuates apoptosis and osteoblastic differentiation of valvular interstitial cells, thus blocking valvular tissue calcification. These findings question a general phase-independent calcific aortic valve disease-promoting role of TGF-β1.
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Braunlin, Elizabeth, Jakub Tolar, Shannon Mackey-Bojack, Tiwanda Marsh, Paul Orchard, and Frederick Schoen. "20. Cardiac valvular interstitial cells in MPS I." Molecular Genetics and Metabolism 99, no. 2 (February 2010): S12. http://dx.doi.org/10.1016/j.ymgme.2009.10.037.

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Sakamoto, Yusuke, and Michael S. Sacks. "An Active Contraction Model of Valvular Interstitial Cells." Biophysical Journal 110, no. 3 (February 2016): 625a. http://dx.doi.org/10.1016/j.bpj.2015.11.3349.

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Immohr, Moritz Benjamin, Helena Lauren Teichert, Fabió dos Santos Adrego, Vera Schmidt, Yukiharu Sugimura, Sebastian Johannes Bauer, Mareike Barth, Artur Lichtenberg, and Payam Akhyari. "Three-Dimensional Bioprinting of Ovine Aortic Valve Endothelial and Interstitial Cells for the Development of Multicellular Tissue Engineered Tissue Constructs." Bioengineering 10, no. 7 (June 30, 2023): 787. http://dx.doi.org/10.3390/bioengineering10070787.

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To investigate the pathogenic mechanisms of calcified aortic valve disease (CAVD), it is necessary to develop a new three-dimensional model that contains valvular interstitial cells (VIC) and valvular endothelial cells (VEC). For this purpose, ovine aortic valves were processed to isolate VIC and VEC that were dissolved in an alginate/gelatin hydrogel. A 3D-bioprinter (3D-Bioplotter® Developer Series, EnvisionTec, Gladbeck, Germany) was used to print cell-laden tissue constructs containing VIC and VEC which were cultured for up to 21 days. The 3D-architecture, the composition of the culture medium, and the hydrogels were modified, and cell viability was assessed. The composition of the culture medium directly affected the cell viability of the multicellular tissue constructs. Co-culture of VIC and VEC with a mixture of 70% valvular interstitial cell and 30% valvular endothelial cell medium components reached the cell viability best tested with about 60% more living cells compared to pure valvular interstitial cell medium (p = 0.02). The tissue constructs retained comparable cell viability after 21 days (p = 0.90) with different 3D-architectures, including a “sandwich” and a “tube” design. Good long-term cell viability was confirmed even for thick multilayer multicellular tissue constructs. The 3D-bioprinting of multicellular tissue constructs with VEC and VIC is a successful new technique to design tissue constructs that mimic the structure of the native aortic valve for research applications of aortic valve pathologies.
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McCoy, Chloe, Dylan Q. Nicholas, and Kristyn S. Masters. "Characterization of Sex-Related Differences in Valvular Interstitial Cells." QScience Proceedings 2012, no. 4 (June 11, 2012): 28. http://dx.doi.org/10.5339/qproc.2012.heartvalve.4.28.

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van Engeland, Nicole C. A., Sergio Bertazzo, Padmini Sarathchandra, Ann McCormack, Carlijn V. C. Bouten, Magdi H. Yacoub, Adrian H. Chester, and Najma Latif. "Aortic calcified particles modulate valvular endothelial and interstitial cells." Cardiovascular Pathology 28 (May 2017): 36–45. http://dx.doi.org/10.1016/j.carpath.2017.02.006.

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Dissertations / Theses on the topic "Valvular interstitial cells"

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Heaney, Allison Mahoney. "Culture and phenotype of canine valvular interstitial cells." Thesis, Manhattan, Kan. : Kansas State University, 2007. http://hdl.handle.net/2097/319.

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Kural, Mehmet Hamdi. "Regulating Valvular Interstitial Cell Phenotype by Boundary Stiffness." Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-dissertations/303.

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"A quantitative understanding of the complex interactions between cells, soluble factors, and the biological and mechanical properties of biomaterials is required to guide cell remodeling towards regeneration of healthy tissue rather than fibrocontractive tissue. The goal of this thesis was to elucidate the interactions between the boundary stiffness of three-dimensional (3D) matrix and soluble factors on valvular interstitial cell (VIC) phenotype with a quantitative approach. The first part of the work presented in this thesis was to characterize the combined effects of boundary stiffness and transforming growth factor-β1 (TGF-β1) on cell-generated forces and collagen accumulation. We first generated a quantitative map of cell-generated tension in response to these factors by culturing VICs within micro-scale fibrin gels between compliant posts (0.15-1.05 nN/nm) in chemically-defined media with TGF-β1 (0-5 ng/mL). The VICs generated 100 to 3000 nN/cell after one week of culture, and multiple regression modeling demonstrated, for the first time, quantitative interaction (synergy) between these factors in a 3D culture system. We then isolated passive and active components of tension within the micro-tissues and found that cells cultured with high levels of stiffness and TGF-β1 expressed myofibroblast markers and generated substantial residual tension in the matrix yet, surprisingly, were not able to generate additional tension in response to membrane depolarization signifying a state of continual maximal contraction. In contrast, negligible residual tension was stored in the low stiffness and TGF-β1 groups indicating a lower potential for shrinkage upon release. We then studied if ECM could be generated under the low tension environment and found that TGF-β1, but not EGF, increased de novo collagen accumulation in both low and high tension environments roughly equally. Combined, these findings suggest that isometric cell force, passive retraction, and collagen production can be tuned by independently altering boundary stiffness and TGF-β1 concentration. In the second part, by using the quantitative information obtained from the first part, we investigated the effects of dynamic changes in stiffness on cell phenotype in a 3D protein matrix, quantitatively. Our novel method utilizing magnetic force to constrain the motion of one of two flexible posts between which VIC-populated micro-tissues were cultured effectively doubled the boundary stiffness and resulted in a significant increase in cell-generated forces. When the magnetic force was removed, the effective boundary stiffness was halved and the tissue tension dropped to 65-87% of the peak value. Surprisingly, following release the cell-generated forces continued to increase for the next two days rather than reducing down to the homeostatic tension level of the control group with identical (but constant) boundary stiffness. The rapid release of tension with the return to baseline boundary stiffness did not result in a decrease in number of cells with α-SMA positive stress fibers or an increase in apoptosis. When samples were entirely released from the boundaries and cultured free floating (where tension is minimal but cannot be measured), the proportion of apoptotic cells in middle region of the micro-tissues increased more than five-fold to 31%. Together, these data indicate that modest temporary changes in boundary stiffness can have lasting effects on myofibroblast activation and persistence in 3D matrices, and that a large decrease in the ability of the cells to generate tension is required to trigger de-differentiation and apoptosis. "
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Hinds, Heather C. "Evaluating terminal differentiation of porcine valvular interstitial cells in vitro." Link to electronic thesis, 2006. http://www.wpi.edu/Pubs/ETD/Available/etd-050506-113014/.

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Cirka, Heather Ann. "Mechanical Regulation of Apoptosis and Calcification within Valvular Interstitial Cells." Digital WPI, 2016. https://digitalcommons.wpi.edu/etd-dissertations/213.

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Calcific aortic valvular disease (CAVD) is the most common valvular pathology in the developed world. CAVD results in calcifications forming on the aortic valve leaflets, inhibiting proper closure and causing complications of stenosis and regurgitation. Although, the mechanisms behind the disease initiation are unknown, it is believed to be a cell-mediated phenomenon, and not the result of passive degradation of the valve as once believed due to the increased prevalence with age. Currently, there are no pharmaceutical options for the prevention or reversal of calcifications, the only treatment option is complete valve replacement, an imperfect solution. Hindering the development of potential therapeutics is that currently there are no adequate animal models which replicate the calcification and cell death seen in disease explanted valves. An in vitro model has been develop where valvular interstitial cells (VICs), the main cell type of the valve, are seeded at high density into tissue culture polystyrene dishes and cultured with TGF-β1. This results in VICs activating to the myofibroblast phenotype and forming cell aggregates. Due to currently unknown mechanisms, apoptosis occurs within the center of the aggregates and calcification ensues. Although simplistic, this model has been used to show that rate and frequency of aggregation is affected by cellular tension; conditions of high tension increase aggregation response, while conditions of low tension prevent aggregation and calcification from occurring. It is important to note; however, that despite its wide usage, the current model is limited as the aggregation and subsequent calcification are random occurrences and are not consistent across literature where same conditions for control samples are used. The motivation of the presented work is two-fold. First, high intracellular tension has been suggested as one of the mechanisms leading to disease in the valve. Despite the clear and important role of cell tension, VIC tension has never before been measured in a dynamic environment. The ways in which dynamic stimulation affects individual VIC tension is not known. In aim one, a method is developed to allow for long-term cyclic stretch of VICs with measurement of cell traction force. It was found that cyclic stretch decreased cell tension in cells with high prestress and increased cell tension for conditions of low prestress. Combined, these findings indicate a homeostatic cellular tension which is dependent upon the mechanical environment. In the second aim, a novel method for creating VIC aggregates is validated. Micro-contact printing, essentially “stampingâ€� of a protein in a defined pattern, is used to create circular aggregates on polyacrylamide gels. This method allows for the separation of the aggregation from the subsequent calcification, an improvement over the current in vitro model. The method is then used to explore the role of the distribution of tension in the initiation of disease
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Shah, Darshita Naresh. "Tailored environments for the three-dimensional culture and manipulation of valvular interstitial cells." Connect to online resource, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3303828.

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Cushing, Melinda Chanel. "Understanding and manipulating extracellular signals critical to the myofibroblast activation of valvular interstitial cells." Connect to online resource, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3256443.

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Aize, Margaux. "Rôle du canal iοnique ΤRΡΜ4 dans la différenciatiοn οstéοgénique des cellules interstitielles de la valve aοrtique humaine." Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC411.

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TRPM4 est un canal cationique non sélectif activé par le calcium intracellulaire impliqué dans le remodelage des fibroblastes cardiaques humains. Ces cellules partagent des caractéristiques communes avec les cellules interstitielles valvulaires (VIC) principales cellules qui composent les valves aortiques, notamment leur capacité de transdifférenciation phénotypique. La différenciation ostéogénique est une étape clé dans la calcification valvulaire menant au rétrécissement aortique calcifié. L’expression du canal TRPM4 est augmentée dans les valves aortiques issues de patients souffrant de rétrécissement aortique calcifié suggérant que le canal TRPM4 peut être impliqué dans les processus de calcification valvulaire. De plus, ce canal est impliqué dans le remodelage valvulaire aortique radio-induit dans un modèle murin. Cependant, à l’heure actuelle les acteurs cellulaires et les mécanismes TRPM4-dépendants impliqués dans ce remodelage demeurent inconnus. Le but de ce travail était de mettre en évidence une potentielle implication de TRPM4 dans la différenciation ostéogénique des VIC humaines (hVIC) et les mécanismes moléculaires impliqués.Ce travail a permis de mettre en évidence que le canal TRPM4 est préférentiellement exprimé à la membrane et une signature électrophysiologique du canal TRPM4 a été enregistrée. TRPM4 est impliqué dans la différenciation ostéogénique des hVIC aussi bien dans les cellules issues de valves calcifiées que dans les hVIC issues de valves non calcifiées. Cet effet passe par l’activation de diverses voies de signalisation, notamment une activation TRPM4-dépendante de la voie BMP2/SMAD1/5 et de la voie NFAT. De plus, nous avons pu observer une plus forte expression du canal TRPM4 dans les hVIC issues de valves calcifiées en comparaison des cellules issues de valves non calcifiées. De même, la culture des hVIC en milieu pro-calcifiant a conduit à une augmentation de l’expression du canal. Enfin, l’irradiation des hVIC à une dose de 8 Gy a entrainé une augmentation de la surface cellulaire associée à une sénescence cellulaire qui est TRPM4-dépendante.Dans l’ensemble, ce travail a permis de mettre en évidence le canal TRPM4 comme un nouvel acteur dans la différenciation des hVIC
TRPM4 is a non-selective cation channel activated by intracellular calcium involved in the remodeling of human cardiac fibroblasts. These cells share properties with the valvular interstitial cells (VIC), the main cells that compose the aortic valves, including their capacity for phenotypic transdifferentiation. Osteogenic differentiation is a key element in valve mineralization leading to calcified aortic stenosis. TRPM4 channel expression is increased in aortic valves from patients with calcified aortic stenosis suggesting that TRPM4 could be involved in the valve’s calcification process. Furthermore, this channel is involved in radiation-induced aortic valve remodeling in mouse. However, the cellular actors and TRPM4-dependant pathways involved in this remodeling remain unknown. The purpose of this study was to search for potential implication of TRPM4 in osteogenic differentiation of human VIC (hVIC) and underlying molecular mechanisms.This work demonstrated that the TRPM4 channel is preferentially expressed at the plasma membrane and a typical electrophysiological signature of TRPM4 was recorded on hVIC. TRPM4 is involved in the osteogenic differentiation of hVIC both in cells originating from calcified valves and in hVIC originating from non-calcified valves. This effect occured through the activation of various signaling pathways, including a TRPM4-dependent activation of the BMP2/SMAD1/5 pathway and the NFAT pathway. Moreover, we were able to observe a stronger expression of the TRPM4 channel in hVIC from calcified valves compared to cells from non-calcified valves. Likewise, the culture of hVIC in a pro-calcifying medium led to an increase in the expression of the channel. Finally, hVIC radiation at a dose of 8 Gy resulted in an increase in cell surface area associated to a cellular senescence which are both TRPM4-dependent.Overall, this work highlights the TRPM4 channel as a new player in the differentiation of hVIC
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Quinlan, Angela. "Mechanical Activation Of Valvular Interstitial Cell Phenotype." Digital WPI, 2012. https://digitalcommons.wpi.edu/etd-dissertations/355.

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"During heart valve remodeling, and in many disease states, valvular interstitial cells (VICs) shift to an activated myofibroblast phenotype which is characterized by enhanced synthetic and contractile activity. Pronounced alpha smooth muscle actin (alpha-SMA)-containing stress fibers, the hallmark of activated myofibroblasts, are also observed when VICs are placed under tension due to altered mechanical loading in vivo or during in vitro culture on stiff substrates or under high mechanical loads and in the presence of transforming growth factor-beta 1 (TGF-beta 1). The work presented herein describes three distinct model systems for application of controlled mechanical environment to VICs cultured in vitro. The first system uses polyacrylamide (PA) gels of defined stiffness to evaluate the response of VICs over a large range of stiffness levels and TGF-beta 1 concentration. The second system controls the boundary stiffness of cell-populated gels using springs of defined stiffness. The third system cyclically stretches soft or stiff two-dimensional (2D) gels while cells are cultured on the gel surface as it is deformed. Through the use of these model systems, we have found that the level of 2D stiffness required to maintain the quiescent VIC phenotype is potentially too low for a material to both act as matrix to support cell growth in the non-activated state and also to withstand the mechanical loading that occurs during the cardiac cycle. Further, we found that increasing the boundary stiffness on a three-dimensional (3D) cell populated collagen gel resulted in increased cellular contractile forces, alpha-SMA expression, and collagen gel (material)stiffness. Finally, VIC morphology is significantly altered in response to stiffness and stretch. On soft 2D substrates, VICs cultured statically exhibit a small rounded morphology, significantly smaller than on stiff substrates. Following equibiaxial cyclic stretch, VICs spread to the extent of cells cultured on stiff substrates, but did not reorient in response to uniaxial stretch to the extent of cells stretched on stiff substrates. These studies provide critical information for characterizing how VICs respond to mechanical stimuli. Characterization of these responses is important for the development of tissue engineered heart valves and contributes to the understanding of the role of mechanical cues on valve pathology and disease onset and progression. While this work is focused on valvular interstitial cells, the culture conditions and methods for applying mechanical stimulation could be applied to numerous other adherent cell types providing information on the response to mechanical stimuli relevant for optimizing cell culture, engineered tissues or fundamental research of disease states."
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Boroomand, Seti. "Valvular interstitial cell transformation : implications for aortic valve calcification." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/47138.

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Aortic valve stenosis (AVS) involves the transformation of valvular interstitial cells (VIC) into an osteoblastic phenotype. Such valvular disease is mostly associated with both thickening and calcification of the valve cusps, which is accompanied by inflammation and remodeling of the tissue. This process is mediated by the VIC that carry out an impressive array of functions throughout the calcification process. For this dissertation, I hypothesized that in AVS, VIC transform from a myofibroblast phenotype to osteoblast-like cells and that the canonical Wnt and TGFβ pathways and vitamin D3 interactively and collaboratively contribute to these phenomena. In order to test this hypothesis, I established an in vitro model of calcification by culturing human primary VIC in a pro-calcification conditioned medium. Calcified cells display several molecular characteristic features of human AVS, including increased levels of alkaline phosphatase and the formation of calcium nodules. These changes increased over time and peaked at 28 days of treatment. To define possible mechanisms of AVS, I first characterized human VIC in regards to the process of calcification. I showed for the first time in vitro that these VIC express bone specific markers, the characteristic of normal osteoblasts. To determine the factors involved in osteoblastic transformation in this model, I examined WNT3A and TGFβ, known to be involved in normal bone formation. Both calcified human aortic valve tissues and VIC express excess WNT3A and TGFβ1. Adding WNT3A and TGFβ1 to the VIC cultures increased the levels of cell mineralization. Further, the addition of DKK1, the WNT3A antagonist, decreased VIC calcification in vitro. By using various combinations of WNT3A, TGFB1 and DKK1, I made the novel observation that the suppression of DKK1 by TGFB1 allowed WNT3A to drive calcification in VIC in vitro. Finally, I examined the role vitamin D3 that is associated with vascular calcification in rats. Vitamin D3 can up-regulate VIC calcification in vitro, however its mechanism of action appears to be independent of the Wnt and TGFβ pathways. In conclusion, the canonical Wnt and TGFβ pathways function interactively through DKK1 to transform VIC to osteoblast-like cells and vitamin D3 promotes this process in an independent manner.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Throm, Quinlan Angela M. "Mechanical Activation of Valvular Interstitial Cell Phenotype: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/640.

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During heart valve remodeling, and in many disease states, valvular interstitial cells (VICs) shift to an activated myofibroblast phenotype which is characterized by enhanced synthetic and contractile activity. Pronounced alpha smooth muscle actin (αSMA)-containing stress fibers, the hallmark of activated myofibroblasts, are also observed when VICs are placed under tension due to altered mechanical loading in vivo or during in vitro culture on stiff substrates or under high mechanical loads and in the presence of transforming growth factor-beta1 (TGF-β1). The work presented herein describes three distinct model systems for application of controlled mechanical environment to VICs cultured in vitro. The first system uses polyacrylamide (PA) gels of defined stiffness to evaluate the response of VICs over a large range of stiffness levels and TGF-β1 concentration. The second system controls the boundary stiffness of cell-populated gels using springs of defined stiffness. The third system cyclically stretches soft or stiff two-dimensional (2D) gels while cells are cultured on the gel surface as it is deformed. Through the use of these model systems, we have found that the level of 2D stiffness required to maintain the quiescent VIC phenotype is potentially too low for a material to both act as matrix to support cell growth in the non-activated state and also to withstand the mechanical loading that occurs during the cardiac cycle. Further, we found that increasing the boundary stiffness on a three-dimensional (3D) cell populated collagen gel resulted in increased cellular contractile forces, αSMA expression, and collagen gel (material) stiffness. Finally, VIC morphology is significantly altered in response to stiffness and stretch. On soft 2D substrates, VICs cultured statically exhibit a small rounded morphology, significantly smaller than on stiff substrates. Following equibiaxial cyclic stretch, VICs spread to the extent of cells cultured on stiff substrates, but did not reorient in response to uniaxial stretch to the extent of cells stretched on stiff substrates. These studies provide critical information for characterizing how VICs respond to mechanical stimuli. Characterization of these responses is important for the development of tissue engineered heart valves and contributes to the understanding of the role of mechanical cues on valve pathology and disease onset and progression. While this work is focused on valvular interstitial cells, the culture conditions and methods for applying mechanical stimulation could be applied to numerous other adherent cell types providing information on the response to mechanical stimuli relevant for optimizing cell culture, engineered tissues or fundamental research of disease states.
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Books on the topic "Valvular interstitial cells"

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Kovanen, Petri T., and Magnus Bäck. Valvular heart disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0015.

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The heart valves, which maintain a unidirectional cardiac blood flow, are covered by endothelial cells and structurally composed by valvular interstitial cells and extracellular matrix. Valvular heart disease can be either stenotic, causing obstruction of the valvular flow, or regurgitant, referring to a back-flow through the valve. The pathophysiological changes in valvular heart disease include, for example, lipid and inflammatory cell infiltration, calcification, neoangiogenesis, and extracellular matrix remodelling. The present chapter addresses the biology of the aortic and mitral valves, and the pathophysiology of aortic stenosis and mitral valve prolapse.
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Dettman, Robert, Juan Antonio Guadix, Elena Cano, Rita Carmona, and Ramón Muñoz-Chápuli. The multiple functions of the proepicardial/epicardial cell lineage in heart development. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0020.

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The epicardium is the outer cell layer of the vertebrate heart. In recent years, both the embryonic and adult epicardium have revealed unsuspected peculiarities and functions, which are essential for cardiac development. In this chapter we review the current literature on the epicardium, and describe its evolutionary origin, the mechanisms leading to the induction of its extracardiac progenitor tissue, the proepicardium, and the way in which the proepicardium is transferred to the heart to form the epicardium. We also describe the epicardial epithelial–mesenchymal transition from which mesenchymal cells originate, and the developmental fate of these cells, which contribute to the vascular, interstitial, valvular, and adipose tissue. Finally, we review the molecular interactions established between the epicardium and the myocardium, which are key for myocardial development and can also play a role in cardiac homeostasis. This chapter highlights how the epicardium has become a major protagonist in cardiac biology.
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Book chapters on the topic "Valvular interstitial cells"

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Ground, Marcus, Karen Callon, Rob Walker, Paget Milsom, and Jillian Cornish. "Valvular Interstitial Cells: Physiology, Isolation, and Culture." In Technologies in Cell Culture - A Journey From Basics to Advanced Applications [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.112649.

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Valvular interstitial cells (VICs) are the primary cellular component of the heart valve. Their function is to maintain the structure of the valve leaflets as they endure some three billion beats in the course of a human lifespan. Valvular pathology is becoming ever more prevalent in our ageing world, and there has never been a greater need for understanding of the pathological processes that underpin these diseases. Despite this, our knowledge of VIC pathology is limited. The scientific enquiry of valve disease necessitates stable populations of VICs in the laboratory. Such populations are commonly isolated from porcine and human tissue. This is achieved by digesting valve tissue from healthy or diseased sources. Understanding of the many VIC phenotypes, and the biochemical cues that govern the transition between phenotypes is essential for experimental integrity. Here we present an overview of VIC physiology, and a tried-and-true method for their isolation and culture. We make mention of several biochemical cues that the researcher may use in their culture media to ensure high quality and stable VIC populations.
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Deepak, Thirumalai, Patina Yamini, and Anju R. Babu. "Biomechanics of the Aortic Valve in Health and Disease." In Advances in Computational Approaches in Biomechanics, 137–52. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-9078-2.ch009.

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The aortic valve is composed of collagen, elastin, proteoglycan, valvular interstitial cells (VIC), and valvular endothelial cells (VEC). In the open condition, the aorta valve allows blood to leave the heart, and in the closed condition, it prevents the backflow of the blood to the left ventricle. However, when the aortic valve cups become narrow or thickened, cusp motion is impaired and obstructs the blood flow. This chapter investigates the structure and composition of the aortic valve cusp and the role of VIC, VEC, and cross-talk of VEC-VIC. In addition, biomechanical characterization of the aortic cusps such as uniaxial, biaxial, flexure, three-point bending, cantilever bending, and viscoelasticity was discussed. Furthermore, etiology, in vitro cell culture and in vivo animal models, and ex vivo models mimicking aortic stenosis and regurgitation were summarized.
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Conference papers on the topic "Valvular interstitial cells"

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Kural, Mehmet H., and Kristen L. Billiar. "Effect of Boundary Stiffness on Contractility Profile of Valvular Interstitial Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14100.

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Heart valve disease leads to approximately 300,000 heart valve replacement surgeries each year worldwide. Valvular interstitial cells (VICs) are believed to play a vital role in the repair of heart valves and also most disease processes. VICs synthesize, remodel, and repair the ECM; however, when VICs excessively differentiate to the highly contractile and synthetic myofibroblast phenotype, valvular fibrosis may ensue. Elevated mechanical stress triggers the differentiation of VICs into myofibroblasts. Transforming growth factor beta-1 (TGF-β1) is also critical for the formation of thicker stress fibers positive for α-smooth muscle actin (α-SMA), the defining characteristic of myofibroblasts.
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Niazy, N., S. Bandar, K. Katsoutas, H. Preuß, D. Saeed, and A. Lichtenberg. "Effects of TGFβ Stimulation in Aortic Valvular Interstitial Cells Are Altered in Hypoxia." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678967.

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Weinberg, Eli, and Mohammad Mofrad. "Multiscale Fluid-Structure Simulations of the Aortic Valve." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176730.

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In the heart aortic valve, maintenance of healthy conditions and transition to diseased conditions are modulated by the cells in the valve. The cells found within the valve leaflets and walls are the valvular interstitial cells (VICs), and those found on the fluid-facing surfaces are the endothelial cells (ECs). Both types of cell are known to respond to their mechanical state; that is, the stresses and deformations imposed on the cell by its surrounding environment. Here, we present a set of simulations to examine the mechanical states of cells as the valve goes through its opening and closing cycle. The simulations span the cell, tissue, and organ length scales. Taken together, these simulations predict the dynamic, three-dimensional mechanical state of VICs and ECs throughout the valve.
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Immohr, M. B., M. Barth, F. Santos, Y. Sugimura, A. Lichtenberg, and P. Akhyari. "3D-Bioprinting of Valvular Interstitial Cells of Ovine Aortic Valves: Impact of Printing Parameters on Cell Viability." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725707.

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Ferdous, Zannatul, Hanjoong Jo, and Robert M. Nerem. "Differential Osteogenic Marker Expression by Human Vascular and Valvular Cells in Tissue-Engineered Collagen Constructs." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19424.

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Atherosclerosis and aortic stenosis are two of the most prevalent cardiovascular disorders and a major cause of death in elderly population. In atherosclerosis, plaques and calcium deposits build up inside major arteries, which lead to narrowing of the vessel lumens and limits or completely blocks blood flow. Similarly, in calcific aortic stenosis, calcium deposits on valve cusps and valve ring result in narrowing of valve lumen, eventually leading to impaired function and even valve failure. As the disease progresses, both diseases thus require expensive replacement/repair surgeries in most patients. However, in spite of the high prevalence, the causes and mechanisms of these diseases are still not clearly understood. Due to the similarities in diseased tissue pathology, atherosclerosis and aortic stenosis have been suggested to be continuum of the same disease [1] and mainly have been investigated for atherosclerosis. However, the prevalence of both diseases is not concurrent in most patients. Likewise, valvular interstitial cells (VICs) were thought to behave in a similar manner as smooth muscle cells (SMCs), but some recent studies suggest differences between the two cell types [2]. Therefore, unique mechanisms might be involved in how VICs and SMCs respond to an osteogenic environment.
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Weinberg, Eli J., and Mohammad R. K. Mofrad. "Multiscale Simulations of the Healthy and Calcific Human Aortic Valve." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192671.

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In the heart’s aortic valve, maintenance of a healthy state and transition to disease states are modulated by the cells in the valve. The cells found within the valve leaflets are valvular interstitial cells (VICs) and those found on the fluid-facing surfaces are endothelial cells (ECs). Both types of cell are known to respond to their mechanical state; that is, the stresses and deformations imposed on a cell by its surrounding environment. Here we present a set of simulations to examine these mechanical states of the cells as the valve goes through its opening and closing cycle. We have created models at each of the cell, tissue, and organ length scales and introduced a system of reference configurations to link the scales. Each simulation and the set of multiscale simulation are verified against experimental data. This multiscale simulation approach allows us to accurately predict the dynamic, three-dimensional mechanical state of cells throughout the valve.
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Carruthers, Christopher A., Bryan Good, Antonio D’Amore, Jun Liao, Rouzbeh Amini, Simon C. Watkins, and Michael S. Sacks. "Alterations in the Microstructure of the Anterior Mitral Valve Leaflet Under Physiological Stress." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80820.

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An improved understanding of mitral valve (MV) function remains an important goal for determining mechanisms underlying valve disease and for developing novel therapies. Critical to heart valve tissue homeostasis is the valvular interstitial cells (VICs), which reside in the interstitium and maintain the extracellular matrix (ECM) through both protein synthesis and enzymatic degradation [1]. There is scant quantitative experimental data on the alterations of the MV fiber network reorganization as a function of load, which is critical for implementation of computational strategies that attempt to link this meso-micro scale phenomenon. The observed large scale deformations experienced by VICs could be implicated in mechanotransduction [2], i.e., translation of mechanical stimuli into biochemical signals. Consequently, our goal was to quantitatively characterize the MV microstructure as a function of physiological loads, including localized 3D VIC deformations and relate it to the fiber network.
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Sewell-Loftin, M. K., Daniel M. DeLaughter, Joey V. Barnett, and W. David Merryman. "Collagen-Hyaluronic Acid Hydrogels Provide Enhanced EMT of Endocardial Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14204.

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A viable tissue engineered heart valve (TEHV) replacement would eliminate disadvantages associated with currently available prosthetics, such as thrombosis and increased risk of valve calcification. Viable TEHVs also are promising in that they can actively remodel and grow, as they would be populated with cells similar to native valves. Valvular interstitial cells (VICs) organize and maintain the complex structure of valves throughout the life of an organism. Considerable effort has been made towards identifying a source of VICs for next generation prosthetic heart valves. Despite this effort, the mechanisms by which VICs are produced in development, via endocardial epithethelial-to-mesenchymal transformation (EMT), are not fully understood. EMT is the critical first step in the formation of heart valve leaflets in utero, and thus a thorough understanding of the biomechanical and signaling environments that regulate EMT could lead to advancements in viable TEHVs.
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Carruthers, Christopher A., Bryan Good, Antonio D’Amore, Rouzbeh Amini, Joseph H. Gorman, and Michael S. Sacks. "Physiological Micromechanics of the Anterior Mitral Valve Leaflet." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53637.

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An improved understanding of mitral valve (MV) function remains an important goal for determining mechanisms underlying valve disease and for developing novel therapies. Critical to heart valve tissue homeostasis is the valvular interstitial cells (VICs), which reside in the interstitium and maintain the extracellular matrix (ECM) through both protein synthesis and enzymatic degradation [1]. There is scant experimental data on the alterations of the MV fiber network reorganization as a function of load, which is critical for implementation of computational strategies that attempt to link this meso-micro scale phenomenon. The observed large scale deformations experienced by VICs could be implicated in mechanotransduction [2], i.e., translation of mechanical stimuli into biochemical signals. Consequently, our goal is to quantitatively connect organ level loads to cellular deformation as a function of the ECM fiber network. We hypothesize that cellular deformations are likely a complex function of collagen and elastin fiber mechanical properties, architecture, and cellular coupling to these fibers.
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Chen, Joseph, Charles I. Fisher, M. K. Sewell-Loftin, and W. David Merryman. "Calcific Nodule Morphogenesis by Aortic Valve Interstitial Cells: Synergism of Applied Strain and TGF-β1." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53899.

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Calcific Aortic Valve Disease (CAVD) is the third most common cause of cardiovascular disease, affecting nearly 5 million people in the United States alone. It is now the most common form of acquired valvular disease in industrialized countries and will likely affect more individuals in the coming years as the prevalence increases with life expectancy. It is known that the progression of CAVD is closely related to the behavior of aortic valve interstitial cells (AVICs); however the cellular mechanobiological mechanisms leading to dysfunction remain unclear. Generally, CAVD is characterized by the formation of calcified AVIC aggregates with an apoptotic core. These aggregates increase the leaflet stiffness and impede normal valve function. Multiple studies have investigated the effects of various biochemical cues on this process, such as transformation growth factor β1 (TGF-β1), on the regulation of nodule formation [1]. Additionally, Yip et al revealed that matrix stiffness controls nodule formation in vitro, with stiffer substrates promoting apoptotic nodule formation, while compliant substrates generated nodules containing cells with osteoblast markers [2]. This suggests that matrix stiffness is involved in the regulatory mechanisms of nodule formation and may initiate different types of nodule formation (i.e. osteogenic vs. dystrophic). In the current study, we examined the synergistic role of strain and TGF-β1 in the generation of calcified nodules AVICs.
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Reports on the topic "Valvular interstitial cells"

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Cushing, Donish, Darshana Goakar, and Bomi Joseph. Higher bioactivity cannabidiol in greater concentration more greatly reduces valvular interstitial cell calcification. Peak Health Center, September 2018. http://dx.doi.org/10.31013/2001f.

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Cushing, Donish, Darshana Goakar, and Bomi Joseph. Bioactive cannabidiol more greatly reduces valvular interstitial cell calcification when combined with ß-Caryophyllene, and α-Humulene. Peak Health Center, September 2018. http://dx.doi.org/10.31013/2001g.

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