Relevant bibliographies by topics / Valve interstitial cells

Contents

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

Academic literature on the topic 'Valve interstitial cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Valve interstitial cells"

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Feng, Yang, Mei Han, and Bin Liu. "The role of valve interstitial cells in valve disease." Anatolian Journal of Cardiology 15, no. 11 (2015): 897–98. http://dx.doi.org/10.5152/anatoljcardiol.2015.17023.

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Latif, Najma, Padmini Sarathchandra, Adrian H. Chester, and Magdi H, Yacoub. "Human Valve Interstitial Cells Demonstrate Transdifferentiation Potential." QScience Proceedings 2012, no. 4 (2012): 18. http://dx.doi.org/10.5339/qproc.2012.heartvalve.4.18.

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Salhiyyah, Kareem, Zamani Marzieh, Padmini Sarathchandra, Najma Latif, Magdi Yacoub, and Adrian H. Chester. "Mitral Valve Interstitial Cells Behaviour Under Hypoxia." QScience Proceedings 2012, no. 4 (2012): 22. http://dx.doi.org/10.5339/qproc.2012.heartvalve.4.22.

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Mulholland, MSc, Diane L., and Avrum I. Gotlieb, MD, CM, FRCP. "Cardiac Valve Interstitial Cells: Regulator of Valve Structure and Function." Cardiovascular Pathology 6, no. 3 (1997): 167–74. http://dx.doi.org/10.1016/s1054-8807(96)00115-9.

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Wu, Bing, Sammy Elmariah, and Emile R. Mohler. "Statins inhibit calcification of aortic valve interstitial cells." Journal of the American College of Cardiology 41, no. 6 (2003): 296. http://dx.doi.org/10.1016/s0735-1097(03)82387-2.

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Gee, Terence, Emily Farrar, Yidong Wang та ін. "NFκB (Nuclear Factor κ-Light-Chain Enhancer of Activated B Cells) Activity Regulates Cell-Type–Specific and Context-Specific Susceptibility to Calcification in the Aortic Valve". Arteriosclerosis, Thrombosis, and Vascular Biology 40, № 3 (2020): 638–55. http://dx.doi.org/10.1161/atvbaha.119.313248.

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Objective: Although often studied independently, little is known about how aortic valve endothelial cells and valve interstitial cells interact collaborate to maintain tissue homeostasis or drive valve calcific pathogenesis. Inflammatory signaling is a recognized initiator of valve calcification, but the cell-type–specific downstream mechanisms have not been elucidated. In this study, we test how inflammatory signaling via NFκB (nuclear factor κ-light-chain enhancer of activated B cells) activity coordinates unique and shared mechanisms of valve endothelial cells and valve interstitial cells d
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Chester, Adrian H., and Patricia M. Taylor. "Molecular and functional characteristics of heart-valve interstitial cells." Philosophical Transactions of the Royal Society B: Biological Sciences 362, no. 1484 (2007): 1437–43. http://dx.doi.org/10.1098/rstb.2007.2126.

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The cells that reside within valve cusps play an integral role in the durability and function of heart valves. There are principally two types of cells found in cusp tissue: the endothelial cells that cover the surface of the cusps and the interstitial cells (ICs) that form a network within the extracellular matrix (ECM) within the body of the cusp. Both cell types exhibit unique functions that are unlike those of other endothelial and ICs found throughout the body. The valve ICs express a complex pattern of cell-surface, cytoskeletal and muscle proteins. They are able to bind to, and communic
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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 (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 int
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Schulz, Alina, Jana Brendler, Orest Blaschuk, Kathrin Landgraf, Martin Krueger, and Albert M. Ricken. "Non-pathological Chondrogenic Features of Valve Interstitial Cells in Normal Adult Zebrafish." Journal of Histochemistry & Cytochemistry 67, no. 5 (2019): 361–73. http://dx.doi.org/10.1369/0022155418824083.

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In the heart, unidirectional blood flow depends on proper heart valve function. As, in mammals, regulatory mechanisms of early heart valve and bone development are shown to contribute to adult heart valve pathologies, we used the animal model zebrafish (ZF, Danio rerio) to investigate the microarchitecture and differentiation of cardiac valve interstitial cells in the transition from juvenile (35 days) to end of adult breeding (2.5 years) stages. Of note, light microscopy and immunohistochemistry revealed major differences in ZF heart valve microarchitecture when compared with adult mice. We d
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Chen, Huiqiang, Wei Cui, Haijuan Hu, and Jing Liu. "Isolation and culture of rat aortic valve interstitial cells." Anatolian Journal of Cardiology 15, no. 11 (2015): 893–96. http://dx.doi.org/10.5152/akd.2014.5817.

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Dissertations / Theses on the topic "Valve interstitial cells"

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Rattazzi, Marcello. "Contribution of Interstitial Valve Cells to Aortic Valve Calcification." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3425639.

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Background. The traditional view of aortic valve calcification as a slow, ineluctable event has been recently questioned by evidence showing the importance of a balance between promoting and inhibiting factors, and the relevance of osteogenic cellular-driven processes. The aortic valve leaflets are comprised of a heterogeneous population of interstitial cells (VIC) whose specific contribution to the degenerating valve has not been defined yet. Aim. The major aim is to identify and describe the phenotypic characteristics of a subpopulation of aortic VIC able to acquire a pro-calcific profile
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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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Salhiyyah, Kareem. "The role of hypoxia on interstitial mitral valve cells." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/41078.

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Mitral valve disease is a multifactorial process. The valve is a complex structure that contains an amalgam of extracellular proteins, cellular components, nerves and blood vessels. It is predicted that some of the central portions of the valve leaflets could exist under hypoxic conditions. Hypoxia could play a role in initiating the structural changes in the valve that lead to dysfunction of the valve. It is known to cause the up-regulation of hypoxia-induced factor (HIF) that can regulate the differentiation of cells, the production of extracellular matrix (ECM) and expression of matrix remo
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Poggio, P. "THE ROLE OF VALVE INTERSTITIAL CELLS IN THE PATHOGENESIS OF CALCIFIC AORTIC VALVE DISEASE." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229415.

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Calcific aortic valve disease (CAVD) is the most common etiology of acquired aortic valve disease. The early stage is characterized by thickening of the leaflets and none or marginal effect on the
mechanical properties of the valve, while the end stage disease is associated with impaired leaflet motion and resistances to blood flow. These conditions are known as aortic valve sclerosis (AVSc) and calcific aortic valve stenosis (AVS), respectively. AVSc is present in 25–30% of patients over 65 years of age and
in up to 40% of those over 75 years of age. Moreover, since AVSc hemodynamics are comp
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Adesanya, T. M. Ayodele. "MG53 protein protects aortic valve interstitial cells from membrane injury and fibrocalcific remodeling." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1534515427092756.

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Butcher, Jonathan Talbot. "The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology." Diss., Georgia Institute of Technology, 2004. http://hdl.handle.net/1853/4824.

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Aortic valve disease (AVD) affects millions of people of all ages around the world. Current treatment for AVD consists of valvular replacement with a non-living prosthetic valve, which is incapable of growth, self-repair, or remodeling. While tissue engineering has great promise to develop a living heart valve alternative, success in animal models has been limited. This may be attributed to the fact that understanding of valvular cell biology has not kept pace with advances in biomaterial development. Aortic valve leaflets are exposed to a complex and dynamic mechanical environment unlike
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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
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Smith, Sally. "Characterisation of the forces generated by human heart valve interstitial cells : relevance to tissue engineering." Thesis, University of Westminster, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434306.

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Liu, Mengmeng. "Tissue-engineered canine mitral valve constructs as in vitro research models for myxomatous mitral valve disease." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/10060.

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Myxomatous mitral valve disease (MMVD) is one of the most common degenerative cardiac diseases affecting humans and dogs; however, its pathogenesis is not completely understood. This study focussed on developing tissue-engineered fibrin based canine mitral valve constructs, which can be used as an in vitro platform to study the pathogenesis of MMVD. Prior to three dimensional (3D) construct fabrication, primary canine mitral valve endothelial cells (VECs) and valve interstitial cells (VICs) were isolated, cultured and characterized utilising a variety of techniques. Moreover, preliminary exper
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Dye, Bailey Katherine. "Cellular Mechanisms of VIC Activation in Mitral Valve Prolapse." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1594995213439086.

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Books on the topic "Valve interstitial cells"

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Fayet, Cristina. Role of cardiac valve interstitial cells in valve repair: Deposition of fibronectin and formation of fibrillar adhesions in response to injury. 2004.

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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,
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Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal in
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Book chapters on the topic "Valve interstitial cells"

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Renato, Millioni, Elisa Bertacco, Cinzia Franchin, Giorgio Arrigoni, and Marcello Rattazzi. "Proteomic Analysis of Interstitial Aortic Valve Cells Acquiring a Pro-calcific Profile." In Methods in Molecular Biology. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-386-2_8.

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Khang, Alex, Rachel M. Buchanan, Salma Ayoub, Bruno V. Rego, Chung-Hao Lee, and Michael S. Sacks. "Biological Mechanics of the Heart Valve Interstitial Cell." In Advances in Heart Valve Biomechanics. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-01993-8_1.

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Khang, Alex, Daniel P. Howsmon, Emma Lejeune, and Michael S. Sacks. "Multi-scale Modeling of the Heart Valve Interstitial Cell." In Multi-scale Extracellular Matrix Mechanics and Mechanobiology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20182-1_2.

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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. 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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Khang, Alex, Rachel M. Buchanan, Salma Ayoub, et al. "Mechanobiology of the heart valve interstitial cell: Simulation, experiment, and discovery." In Mechanobiology in Health and Disease. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-812952-4.00008-8.

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"The Future and Electrogastrography." In Handbook of Electrogastrography, edited by Kenneth L. Koch and Robert M. Stern. Oxford University Press, 2003. http://dx.doi.org/10.1093/oso/9780195147889.003.0013.

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The 3-cycles per minute (cpm) gastric pacesetter potential is a fundamental electrical phenomenon of the stomach. This low-frequency biorhythm is the basis for normal neuromuscular function of the stomach. In regard to the origins and the various neural and hormonal influences that affect the 3-cpm rhythm, many mysteries remain. Ongoing and future inquiries into the very nature of rhythmicity will provide deeper understanding of gastric myoelectrical activity and the electrical activity detected in the electrogastrogram (EGG). The role of knockout mice that lack interstitial cells of Cajal will be increasingly important in understanding the crucial role of rhythmic electrical events in normal and abnormal neuromuscular function of the stomach. These and other animal studies will also continue to help clinicians understand the deficits in gastric neuromuscular function caused by electrical dysrhythmias. A delicate balance maintains normal 3-cpm activity. Stomach electrical rhythmicity is rather unstable during fasting, for example, compared with the rhythmic 3-cpm electrical events and contractile events that occur in the postprandial period. What mechanisms produce these fasting and postprandial electrical changes? Are neural or hormonal circuits most critical? Are extrinsic or intrinsic nerves the most important? Studies of fasting and postprandial EGG activity may offer insights into sensations of hunger and satiety. The EGG signal is responsive to brain-gut interactions such as the cephalic-vagal reflex. Sham feeding studies with healthy subjects indicated that the sight, smell, and taste of food significantly increased 3- cpm activity. However, in subjects who indicated that the sham feeding experience was disgusting, no increase in 3-cpm activity occurred in this situation. Future studies of patients with eating disorders such as bulimia or anorexia nervosa using EGG recording methods may reveal new insights into the pathophysiology of eating disorders and be of value in monitoring the progress of treatment. Different EGG patterns induced by different meals reflect the different gastric neuromuscular work required to receive, mix, and empty the specific meal. Characteristics of the EGG signal from frequency to amplitude may also correlate with perceptions of stomach fullness, hunger, or satiety.
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Conference papers on the topic "Valve interstitial cells"

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Merryman, W. David, Paul D. Bieniek, Farshid Guilak, and Michael S. Sacks. "Aortic Valve Interstitial Cell Viscoelasticity." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176694.

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Long term tissue-level durability of the aortic valve (AV) is maintained by the cell populations residing both in the interstitium and on the epithelium. Due to the dynamic environment in which the AV interstitial cells (AVICs) function, recent work has examined the mechano-dependent, biosynthetic and contractile response of these cells [1–4]. Many idealized assumptions have been made about mechanical properties [1, 4], ECM connectivity [2], and deformations that the AVICs undergo during diastole [3]. These assumptions include that the AVICs are elastic, homogenous materials that deformation i
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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 closin
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Hutcheson, Joshua D., and W. David Merryman. "Serotonin Antagonists Prevent Cytokine and Mechanical Activation of Aortic Valve Interstitial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19389.

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Degenerative aortic valve disease (DAVD) is the most common heart valve pathology and is especially prevalent in the elderly population. Studies have shown that stenosis, the most severe form of DAVD, increases in prevalence from 0.7% in people between 18 and 44 years of age to over 13% of people over 75 years of age. Furthermore, early symptoms of DAVD have been detected in 29% of patients over 65 years of age. These symptoms are associated with a 50% increase in cardiovascular related morbidity and a similar increase in the risk of myocardial infarction [1]. Currently, aortic valve (AV) repl
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Zhao, Ruogang, Lina Lin, and Craig A. Simmons. "The Effects of Cell Contraction and Loss of Adhesion on the Apoptosis of Valve Interstitial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19249.

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Dystrophic calcification in sclerotic aortic valves is associated with apoptosis of myofibroblasts that differentiate from valve interstitial cells (VICs). The factors that regulate apoptosis in sclerotic valves are not known, but may include mechanical stimuli, as is the case in other fibrotic tissues. In support of this hypothesis, we have observed that VICs on stiff collagen matrices that simulate fibrotic tissue differentiate to myofibroblasts and form calcified aggregates that contain apoptotic cells [1]. However, the mechanisms by which cell aggregation leads to VIC apoptosis are unknown
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Hutcheson, Joshua D., M. K. Sewell-Loftin, and W. David Merryman. "Strain and Substrate Stiffness Affect Calcium Accumulation in Aortic Valve Interstitial Cells." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53611.

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The progression of aortic valve (AV) disease is often characterized by the formation of calcific nodules on thickened AV leaflets, limiting the biomechanical function of the valve. Calcification is a major problem that often leads to the failure of bioprosthetic replacement valves [1]. In these cases, the association of extracellular Ca2+ with phosphates remaining in cellular debris within the decellularized scaffolds has been proposed to lead to the nucleation and growth of Ca3(PO4)2 nodules. In native tissue, calcification is thought to be a more active process involving AV interstitial cell
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Chen, Joseph, Joshua D. Hutcheson, M. K. Sewell-Loftin, Larisa M. Ryzhova, Charles I. Fisher, and W. David Merryman. "Cadherin-11 Regulates Calcific Nodule Formation by Aortic Valve Interstitial Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14201.

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Calcific aortic valve disease (CAVD) is characterized by the stiffening and calcification of the aortic valve leaflets which result in impaired valve function and increased load on the myocardium. In vitro models of CAVD involve the formation the calcific nodules via aortic valve interstitial cells (AVICs). Transforming growth factor β1 (TGF-β1) induced myofibroblast differentiation of AVICs, which is evidenced by increased αSMA expression, has been shown to be a key mediator of dystrophic calcific nodule formation. Benton et al. demonstrated the critical role of αSMA in nodule formation in th
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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 str
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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 creat
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Liu, Haijiao, Craig A. Simmons, and Yu Sun. "Characterization of the Elasticity of Valve Interstitial Cells on Soft Substrates Using Atomic Force Microscopy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80369.

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Mechanical stimuli, including the elasticity of the extracellular matrix (ECM), can have profound effects on the function of cells and their responsiveness to other microenvironmental cues, thereby regulating homeostasis and disease development. For example, the response of aortic valve interstitial cells (VICs) to growth factors [1] and VIC differentiation to pathological phenotypes [2] depend on ECM elasticity. The ability of cells to sense and respond to mechanical stimuli depends on several factors, including their inherent cellular-level mechanical properties. The mechanical properties of
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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
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