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Journal articles on the topic 'Valvular interstitial cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 23 November 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Delwarde, C., S. Lecointe, P. Aumond, J. J. Schott, T. Le Tourneau, J. Merot, and R. Capoulade. "Myofibroblastic differentiation of rat valvular interstitial cells in culture." Archives of Cardiovascular Diseases Supplements 12, no. 2-4 (October 2020): 250. http://dx.doi.org/10.1016/j.acvdsp.2020.03.122.

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12

Zhou, Jingxin, Jinfu Zhu, Li Jiang, Busheng Zhang, Dan Zhu, and Yanhu Wu. "Interleukin 18 promotes myofibroblast activation of valvular interstitial cells." International Journal of Cardiology 221 (October 2016): 998–1003. http://dx.doi.org/10.1016/j.ijcard.2016.07.036.

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13

Hmadeh, S., A. Trimaille, M. Kensuke, B. Marchandot, A. Carmona, F. Zobairi, S. Kikuchi, et al. "Impact of valvular interstitial cells-derived microparticles on valvular endothelial cell activation and thrombogenicity." Archives of Cardiovascular Diseases 117, no. 1 (January 2024): S105—S106. http://dx.doi.org/10.1016/j.acvd.2023.10.196.

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14

Vadana, Mihaela, Sergiu Cecoltan, Letitia Ciortan, Razvan D. Macarie, Andreea C. Mihaila, Monica M. Tucureanu, Ana-Maria Gan, et al. "Parathyroid Hormone Induces Human Valvular Endothelial Cells Dysfunction That Impacts the Osteogenic Phenotype of Valvular Interstitial Cells." International Journal of Molecular Sciences 23, no. 7 (March 29, 2022): 3776. http://dx.doi.org/10.3390/ijms23073776.

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Parathyroid hormone (PTH) is a key regulator of calcium, phosphate and vitamin D metabolism. Although it has been reported that aortic valve calcification was positively associated with PTH, the pathophysiological mechanisms and the direct effects of PTH on human valvular cells remain unclear. Here we investigated if PTH induces human valvular endothelial cells (VEC) dysfunction that in turn could impact the switch of valvular interstitial cells (VIC) to an osteoblastic phenotype. Human VEC exposed to PTH were analyzed by qPCR, western blot, Seahorse, ELISA and immunofluorescence. Our results showed that exposure of VEC to PTH affects VEC metabolism and functions, modifications that were accompanied by the activation of p38MAPK and ERK1/2 signaling pathways and by an increased expression of osteogenic molecules (BMP-2, BSP, osteocalcin and Runx2). The impact of dysfunctional VEC on VIC was investigated by exposure of VIC to VEC secretome, and the results showed that VIC upregulate molecules associated with osteogenesis (BMP-2/4, osteocalcin and TGF-β1) and downregulate collagen I and III. In summary, our data show that PTH induces VEC dysfunction, which further stimulates VIC to differentiate into a pro-osteogenic pathological phenotype related to the calcification process. These findings shed light on the mechanisms by which PTH participates in valve calcification pathology and suggests that PTH and the treatment of hyperparathyroidism represent a therapeutic strategy to reduce valvular calcification.

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15

Jana, Soumen, Rebecca Hennessy, Federico Franchi, Melissa Young, Ryan Hennessy, and Amir Lerman. "Regeneration ability of valvular interstitial cells from diseased heart valve leaflets." RSC Advances 6, no. 115 (2016): 113859–70. http://dx.doi.org/10.1039/c6ra24282k.

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Valvular interstitial cells from diseased aortic valve leaflets show their ability to regenerate–to proliferate and grow, to express appropriate genes and to deposit suitable proteins–in a non-degenerative nanofibrous substrate.

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16

Bowler, Meghan A., Matthew R. Bersi, Larisa M. Ryzhova, Rachel J. Jerrell, Aron Parekh, and W. David Merryman. "Cadherin-11 as a regulator of valve myofibroblast mechanobiology." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (December 1, 2018): H1614—H1626. http://dx.doi.org/10.1152/ajpheart.00277.2018.

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Cadherin-11 (CDH11) is upregulated in a variety of fibrotic diseases, including arthritis and calcific aortic valve disease. Our recent work has identified CDH11 as a potential therapeutic target and shown that treatment with a CDH11 functional blocking antibody can prevent hallmarks of calcific aortic valve disease in mice. The present study investigated the role of CDH11 in regulating the mechanobiological behavior of valvular interstitial cells believed to cause calcification. Aortic valve interstitial cells were harvested from Cdh11+/+, Cdh11+/−, and Cdh11−/− immortomice. Cells were subjected to inflammatory cytokines transforming growth factor (TGF)-β1 and IL-6 to characterize the molecular mechanisms by which CDH11 regulates their mechanobiological changes. Histology was performed on aortic valves from Cdh11+/+, Cdh11+/−, and Cdh11−/− mice to identify key responses to CDH11 deletion in vivo. We showed that CDH11 influences cell behavior through its regulation of contractility and its ability to bind substrates via focal adhesions. We also show that transforming growth factor-β1 overrides the normal relationship between CDH11 and smooth muscle α-actin to exacerbate the myofibroblast disease phenotype. This phenotypic switch is potentiated through the IL-6 signaling axis and could act as a paracrine mechanism of myofibroblast activation in neighboring aortic valve interstitial cells in a positive feedback loop. These data suggest CDH11 is an important mediator of the myofibroblast phenotype and identify several mechanisms by which it modulates cell behavior. NEW & NOTEWORTHY Cadherin-11 influences valvular interstitial cell contractility by regulating focal adhesions and inflammatory cytokine secretion. Transforming growth factor-β1 overrides the normal balance between cadherin-11 and smooth muscle α-actin expression to promote a myofibroblast phenotype. Cadherin-11 is necessary for IL-6 and chitinase-3-like protein 1 secretion, and IL-6 promotes contractility. Targeting cadherin-11 could therapeutically influence valvular interstitial cell phenotypes in a multifaceted manner.

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17

Kwan, Kin Ming, Pak Lun Baggio Liu, and Ka Kui Tong. "Valvular endothelial cells are recruited into interstitial cells for heart valve homeostasis." Mechanisms of Development 145 (July 2017): S150. http://dx.doi.org/10.1016/j.mod.2017.04.423.

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18

Blevins, Tracy L., Sherket B. Peterson, Elaine L. Lee, Annie M. Bailey, Jonathan D. Frederick, Thanh N. Huynh, Vishal Gupta, and K. Jane Grande-Allen. "Mitral Valvular Interstitial Cells Demonstrate Regional, Adhesional, and Synthetic Heterogeneity." Cells Tissues Organs 187, no. 2 (2008): 113–22. http://dx.doi.org/10.1159/000108582.

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19

Weber, A., K. Dakaras, M. Barth, K. Baier, J. Schrader, A. Lichtenberg, and P. Akhyari. "Elevated ATP Levels Promote the Mineralization of Valvular Interstitial Cells." Thoracic and Cardiovascular Surgeon 65, S 01 (February 3, 2017): S1—S110. http://dx.doi.org/10.1055/s-0037-1598848.

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20

Ulloa Severino, Luisa, Rosaria Santoro, Maurizio Pesce, Loredana Casalis, and Denis Scaini. "Substrate Chemistry and Morphology Influence the Valvular Interstitial Cells Mechanobiology." Biophysical Journal 112, no. 3 (February 2017): 437a. http://dx.doi.org/10.1016/j.bpj.2016.11.2331.

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21

Yeh, Chiou-Yueh, Chia-Tung Shun, Yu-Min Kuo, Chiau-Jing Jung, Song-Chou Hsieh, Yen-Ling Chiu, Jeng-Wei Chen, Ron-Bin Hsu, Chia-Ju Yang, and Jean-San Chia. "Activated Human Valvular Interstitial Cells Sustain Interleukin-17 Production To Recruit Neutrophils in Infective Endocarditis." Infection and Immunity 83, no. 6 (March 16, 2015): 2202–12. http://dx.doi.org/10.1128/iai.02965-14.

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The mechanisms that underlie valvular inflammation in streptococcus-induced infective endocarditis (IE) remain unclear. We previously demonstrated that streptococcal glucosyltransferases (GTFs) can activate human heart valvular interstitial cells (VIC) to secrete interleukin-6 (IL-6), a cytokine involved in T helper 17 (Th17) cell differentiation. Here, we tested the hypothesis that activated VIC can enhance neutrophil infiltration through sustained IL-17 production, leading to valvular damage. To monitor cytokine and chemokine production, leukocyte recruitment, and the induction or expansion of CD4+CD45RA−CD25−CCR6+Th17 cells, primary human VIC were culturedin vitroand activated by GTFs. Serum cytokine levels were measured using an enzyme-linked immunosorbent assay (ELISA), and neutrophils and Th17 cells were detected by immunohistochemistry in infected valves from patients with IE. The expression of IL-21, IL-23, IL-17, and retinoic acid receptor-related orphan receptor C (Rorc) was upregulated in GTF-activated VIC, which may enhance the proliferation of memory Th17 cells in an IL-6-dependent manner. Many chemokines, including chemokine (C-X-C motif) ligand 1 (CXCL1), were upregulated in GTF-activated VIC, which might recruit neutrophils and CD4+T cells. Moreover, CXCL1 production in VIC was induced in a dose-dependent manner by IL-17 to enhance neutrophil chemotaxis. CXCL1-expressing VIC and infiltrating neutrophils could be detected in infected valves, and serum concentrations of IL-17, IL-21, and IL-23 were increased in patients with IE compared to healthy donors. Furthermore, elevated serum IL-21 levels have been significantly associated with severe valvular damage, including rupture of chordae tendineae, in IE patients. Our findings suggest that VIC are activated by bacterial modulins to recruit neutrophils and that such activities might be further enhanced by the production of Th17-associated cytokines. Together, these factors can amplify the release of neutrophilic contentsin situ, which might lead to severe valvular damage.

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22

Polley, Anisha, Riffat Khanam, Arunima Sengupta, and Santanu Chakraborty. "Asporin Reduces Adult Aortic Valve Interstitial Cell Mineralization Induced by Osteogenic Media and Wnt Signaling Manipulation In Vitro." International Journal of Cell Biology 2020 (April 10, 2020): 1–19. http://dx.doi.org/10.1155/2020/2045969.

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Worldwide, calcific aortic valve disease is one of the leading causes of morbidity and mortality among patients with cardiac abnormalities. Aortic valve mineralization and calcification are the key events of adult calcific aortic valve disease manifestation and functional insufficiency. Due to heavy mineralization and calcification, adult aortic valvular cusps show disorganized and dispersed stratification concomitant with deposition of calcific nodules with severely compromised adult valve function. Interestingly, shared gene regulatory pathways are identified between bone-forming cells and heart valve cells during development. Asporin, a small leucine-rich proteoglycan (43 kDa), acts to inhibit mineralization in periodontal ligament cells and is also detected in normal murine adult aortic valve leaflets with unknown function. Therefore, to understand the Asporin function in aortic cusp mineralization and calcification, adult avian aortic valvular interstitial cell culture system is established and osteogenesis has been induced in these cells successfully. Upon induction of osteogenesis, reduced expression of Asporin mRNA and increased expression of bone and osteogenesis markers are detected compared to cells maintained without osteogenic induction. Importantly, treatment with human recombinant Asporin protein reduces the mineralization level in osteogenic media-induced aortic valvular interstitial cells with the concomitant decreased level of Wnt/β-catenin signaling. Overall, all these data are highly indicative that Asporin might be a novel biomolecular target to treat patients of calcific aortic valve disease over current cusp replacement surgery.

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23

Kwon, Jennie H., Miriam Atteya, Alekhya Mitta, Andrew D. Vogel, Russell A. Norris, and Taufiek Konrad Rajab. "Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells." Journal of Cardiovascular Development and Disease 10, no. 10 (October 19, 2023): 436. http://dx.doi.org/10.3390/jcdd10100436.

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Ischemia–reperfusion injury (IRI) in the myocardium has been thoroughly researched, especially in acute coronary syndrome and heart transplantation. However, our understanding of IRI implications on cardiac valves is still developing. This knowledge gap becomes even more pronounced given the advent of partial heart transplantation, a procedure designed to implant isolated human heart valves in young patients. This study aims to investigate the effects of IRI on aortic valvular endothelial cells (VECs), valvular interstitial cells (VICs), and whole leaflet cultures (no separation of VECs and VICs). We employed two conditions: hypoxic cold storage reperfusion (HCSR) and normothermia (NT). Key markers, secreted protein acidic and cysteine rich (SPARC) (osteonectin), and inducible nitric oxide synthase (iNOS2) were evaluated. In the isolated cells under HCSR, VICs manifested a significant 15-fold elevation in SPARC expression compared to NT (p = 0.0016). Conversely, whole leaflet cultures exhibited a 1-fold increment in SPARC expression in NT over HCSR (p = 0.0011). iNOS2 expression in VECs presented a marginal rise in HCSR, whereas, in whole leaflet settings, there was a 1-fold ascent in NT compared to HCSR (p = 0.0003). Minor escalations in the adhesion molecules intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM), E-selection, and P-selection were detected in HCSR for whole leaflet cultures, albeit without statistical significance. Additionally, under HCSR, VICs released a markedly higher quantity of IL-6 and IL-8, with respective p-values of 0.0033 and <0.0001. Interestingly, the IL-6 levels in VECs remained consistent across both HCSR and NT conditions. These insights lay the groundwork for understanding graft IRI following partial heart transplantation and hint at the interdependent dynamic of VECs and VICs in valvular tissue.

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Nanduri, Vibudha, Beheita Moein, Avinash Raj Thatipalli, Gopal Pande, and Anasuya Ganguly. "Histochemical and Molecular Characterization of Spongiosal Cells in Native Tissue, Two- and Three-Dimensional Cultures of Rat Aortic Valve." Journal of Histology 2016 (January 4, 2016): 1–8. http://dx.doi.org/10.1155/2016/7680701.

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The histocytochemical and molecular analysis of cells that constitute the aortic valve (AV) of the rat heart was done in this study. We have focussed on the identity of cells in the spongiosal layer of the valve by immunofluorescence studies using lineage specific markers and cytochemical staining. We have established two-dimensional (2D) cultures of cells from isolated rat AV leaflets and maintained endothelial and interstitial valvular cells (IVC) over a period of six to eight weeks. Using “passage 0” cells from 2D valvular cultures, we could reconstruct the three-dimensional (3D) valvular tissue in collagen gels that showed very similar cellular organization and marker expression profile, as that of the native tissue. Lineage specific markers in the native tissue and cell cultures were studied by Reverse Transcriptase-PCR and immunofluorescence for VCAM-I, α-SMA, collagen I, CD71, collagen II, and E-cadherin markers. This is the first report on the identification of cell lineages in the spongiosal layer of AV and the successful reconstruction of 3D valvular tissue from primary cell cultures of AV.

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Schlotter, Florian, Arda Halu, Shinji Goto, Mark C. Blaser, Simon C. Body, Lang H. Lee, Hideyuki Higashi, et al. "Spatiotemporal Multi-Omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving Disease." Circulation 138, no. 4 (July 24, 2018): 377–93. http://dx.doi.org/10.1161/circulationaha.117.032291.

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Background: No pharmacological therapy exists for calcific aortic valve disease (CAVD), which confers a dismal prognosis without invasive valve replacement. The search for therapeutics and early diagnostics is challenging because CAVD presents in multiple pathological stages. Moreover, it occurs in the context of a complex, multi-layered tissue architecture; a rich and abundant extracellular matrix phenotype; and a unique, highly plastic, and multipotent resident cell population. Methods: A total of 25 human stenotic aortic valves obtained from valve replacement surgeries were analyzed by multiple modalities, including transcriptomics and global unlabeled and label-based tandem-mass-tagged proteomics. Segmentation of valves into disease stage–specific samples was guided by near-infrared molecular imaging, and anatomic layer-specificity was facilitated by laser capture microdissection. Side-specific cell cultures were subjected to multiple calcifying stimuli, and their calcification potential and basal/stimulated proteomes were evaluated. Molecular (protein–protein) interaction networks were built, and their central proteins and disease associations were identified. Results: Global transcriptional and protein expression signatures differed between the nondiseased, fibrotic, and calcific stages of CAVD. Anatomic aortic valve microlayers exhibited unique proteome profiles that were maintained throughout disease progression and identified glial fibrillary acidic protein as a specific marker of valvular interstitial cells from the spongiosa layer. CAVD disease progression was marked by an emergence of smooth muscle cell activation, inflammation, and calcification-related pathways. Proteins overrepresented in the disease-prone fibrosa are functionally annotated to fibrosis and calcification pathways, and we found that in vitro, fibrosa-derived valvular interstitial cells demonstrated greater calcification potential than those from the ventricularis. These studies confirmed that the microlayer-specific proteome was preserved in cultured valvular interstitial cells, and that valvular interstitial cells exposed to alkaline phosphatase–dependent and alkaline phosphatase–independent calcifying stimuli had distinct proteome profiles, both of which overlapped with that of the whole tissue. Analysis of protein–protein interaction networks found a significant closeness to multiple inflammatory and fibrotic diseases. Conclusions: A spatially and temporally resolved multi-omics, and network and systems biology strategy identifies the first molecular regulatory networks in CAVD, a cardiac condition without a pharmacological cure, and describes a novel means of systematic disease ontology that is broadly applicable to comprehensive omics studies of cardiovascular diseases.

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LIU, Yan-ling, Xiao-hong LIU, De-jun GONG, Yang YUAN, Jing TAO, Sheng-dong HUANG, and Lin HAN. "Biological characteristics of valvular interstitial cells in calcific aortic valve disease." Academic Journal of Second Military Medical University 31, no. 6 (October 24, 2011): 617–20. http://dx.doi.org/10.3724/sp.j.1008.2011.00617.

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Ground, Marcus, Steve Waqanivavalagi, Young-Eun Park, Karen Callon, Robert Walker, Paget Milsom, and Jillian Cornish. "Fibroblast growth factor 2 inhibits myofibroblastic activation of valvular interstitial cells." PLOS ONE 17, no. 6 (June 17, 2022): e0270227. http://dx.doi.org/10.1371/journal.pone.0270227.

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Heart valve disease is a growing problem worldwide. Though very common in older adults, the mechanisms behind the development of the disease aren’t well understood, and at present the only therapeutic option is valve replacement. Valvular interstitial cells (VICs) may hold the answer. These cells can undergo pathological differentiation into contractile myofibroblasts or osteoblasts, leading to thickening and calcification of the valve tissue. Our study aimed to characterise the effect of fibroblast growth factor 2 (FGF-2) on the differentiation potential of VICs. We isolated VICs from diseased human valves and treated these cells with FGF-2 and TGF-β to elucidate effect of these growth factors on several myofibroblastic outcomes, in particular immunocytochemistry and gene expression. We used TGF-β as a positive control for myofibroblastic differentiation. We found that FGF-2 promotes a ‘quiescent-type’ morphology and inhibits the formation of α-smooth muscle actin positive myofibroblasts. FGF-2 reduced the calcification potential of VICs, with a marked reduction in the number of calcific nodules. FGF-2 interrupted the ‘canonical’ TGF-β signalling pathway, reducing the nuclear translocation of the SMAD2/3 complex. The panel of genes assayed revealed that FGF-2 promoted a quiescent-type pattern of gene expression, with significant downregulations in typical myofibroblast markers α smooth muscle actin, extracellular matrix proteins, and scleraxis. We did not see evidence of osteoblast differentiation: neither matrix-type calcification nor changes in osteoblast associated gene expression were observed. Our findings show that FGF-2 can reverse the myofibroblastic phenotype of VICs isolated from diseased valves and inhibit the calcification potential of these cells.

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Vercelli, Cristina, Graziana Gambino, Michela Amadori, Giovanni Re, Eugenio Martignani, Rossella V. Barberis, Izabela Janus, and Massimiliano Tursi. "TRPV1 Receptor Identification in Bovine and Canine Mitral Valvular Interstitial Cells." Veterinary Sciences 8, no. 9 (September 4, 2021): 183. http://dx.doi.org/10.3390/vetsci8090183.

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Myxomatous mitral valve degeneration (MMVD) is the most common acquired cardiac disease in canine species, and valvular interstitial cells (VICs) are considered the main responsible for the development of this pathology. The scientific interest is focused on isolating and characterizing these cells. The aims of the present study were to verify a novel VICs mechanical isolation method and to characterize isolated cells using immunocytochemistry and immunofluorescence, with parallel histological and immunohistochemistry assays on bovine and canine healthy and MMVD mitral valves. Antibodies against vimentin (VIM), smooth muscle actin (SMA), von Willebrand (vW) factor, Transforming Growth Factor (TGF) β1, and Transient Receptor Potential Vanilloid 1 (TRPV1) were used. The isolation method was considered reliable and able to isolate only VICs. The different assays demonstrated a different expression of SMA in healthy and MMVD mitral valves, and TRPV1 was isolated for the first time from bovine and canine VICs and the correspondent mitral valve leaflets. The novelties of the present study are the new isolation method, that may allow correlations between laboratory and clinical conditions, and the identification of TRPV1, which will lead to further investigations to understand its function and possible role in the etiology of MMVD and to the design of new therapeutic strategies.

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Levesque, T., N. Perzo, E. Berg, H. Messaoudi, A. Herbet, B. Colleville, A. Dumesnil, et al. "Calcification of aortic valvular interstitial cells induced by endothelin receptor blockers." Archives of Cardiovascular Diseases Supplements 13, no. 2 (May 2021): 222. http://dx.doi.org/10.1016/j.acvdsp.2021.04.180.

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van Rijswijk, Jan Willem, Pinak Samal, Inge van der Made, Roman Truckenmüller, Stefan Giselbrecht, and Jolanda Kluin. "A Novel Microwell Array for 3D Culture of Valvular Interstitial Cells." Structural Heart 3, sup1 (April 9, 2019): 97. http://dx.doi.org/10.1080/24748706.2019.1590104.

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Heaney, Allison M., Barret J. Bulmer, Christopher R. Ross, and Thomas Schermerhorn. "A technique for in vitro culture of canine valvular interstitial cells." Journal of Veterinary Cardiology 11, no. 1 (June 2009): 1–7. http://dx.doi.org/10.1016/j.jvc.2009.03.005.

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Aize, Margaux, Harlyne Mpweme Bangando, Laura Brard, Arthur Boileve, Vladimir Saplacan, Alexandre Lebrun, Nicolas Perzo, Alain Manrique, Romain Guinamard, and Christophe Simard. "TRPM4: New actor in osteogenic differentiation of human valvular interstitial cells." Archives of Cardiovascular Diseases Supplements 15, no. 2 (May 2023): 219–20. http://dx.doi.org/10.1016/j.acvdsp.2023.03.091.

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Cirka, Heather A., Johana Uribe, Vivian Liang, Frederick J. Schoen, and Kristen L. Billiar. "Reproducible in vitro model for dystrophic calcification of cardiac valvular interstitial cells: insights into the mechanisms of calcific aortic valvular disease." Lab on a Chip 17, no. 5 (2017): 814–29. http://dx.doi.org/10.1039/c6lc01226d.

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Adhikari, Radhika, Saugat Shiwakoti, Ju-Young Ko, Bikalpa Dhakal, Sin-Hee Park, Ik Jun Choi, Hyun Jung Kim, and Min-Ho Oak. "Oxidative Stress in Calcific Aortic Valve Stenosis: Protective Role of Natural Antioxidants." Antioxidants 11, no. 6 (June 14, 2022): 1169. http://dx.doi.org/10.3390/antiox11061169.

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Calcific aortic valve stenosis (CAVS) is the most prevalent heart valvular disease worldwide and a slowly progressive disorder characterized by thickening of the aortic valve, calcification, and subsequent heart failure. Valvular calcification is an active cell regulation process in which valvular interstitial cells involve phenotypic conversion into osteoblasts/chondrocytes-like cells. The underlying pathophysiology is complicated, and there have been no pharmacological treatments for CAVS to date. Recent studies have suggested that an increase in oxidative stress is the major trigger of CAVS, and natural antioxidants could ameliorate the detrimental effects of reactive oxygen species in the pathogenesis of CAVS. It is imperative to review the current findings regarding the role of natural antioxidants in CAVS, as they can be a promising therapeutic approach for managing CAVS, a disorder currently without effective treatment. This review summarizes the current findings on molecular mechanisms associated with oxidative stress in the development of valvular calcification and discusses the protective roles of natural antioxidants in the prevention and treatment of CAVS.

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35

Hénaut, Candellier, Boudot, Grissi, Mentaverri, Choukroun, Brazier, Kamel, and Massy. "New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease." Toxins 11, no. 9 (September 12, 2019): 529. http://dx.doi.org/10.3390/toxins11090529.

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Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.

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Kamel, Peter I., Xin Qu, Andrew M. Geiszler, Deepak Nagrath, Romain Harmancey, Heinrich Taegtmeyer, and K. Jane Grande-Allen. "Metabolic regulation of collagen gel contraction by porcine aortic valvular interstitial cells." Journal of The Royal Society Interface 11, no. 101 (December 6, 2014): 20140852. http://dx.doi.org/10.1098/rsif.2014.0852.

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Despite a high incidence of calcific aortic valve disease in metabolic syndrome, there is little information about the fundamental metabolism of heart valves. Cell metabolism is a first responder to chemical and mechanical stimuli, but it is unknown how such signals employed in valve tissue engineering impact valvular interstitial cell (VIC) biology and valvular disease pathogenesis. In this study porcine aortic VICs were seeded into three-dimensional collagen gels and analysed for gel contraction, lactate production and glucose consumption in response to manipulation of metabolic substrates, including glucose, galactose, pyruvate and glutamine. Cell viability was also assessed in two-dimensional culture. We found that gel contraction was sensitive to metabolic manipulation, particularly in nutrient-depleted medium. Contraction was optimal at an intermediate glucose concentration (2 g l −1 ) with less contraction with excess (4.5 g l −1 ) or reduced glucose (1 g l −1 ). Substitution with galactose delayed contraction and decreased lactate production. In low sugar concentrations, pyruvate depletion reduced contraction. Glutamine depletion reduced cell metabolism and viability. Our results suggest that nutrient depletion and manipulation of metabolic substrates impacts the viability, metabolism and contractile behaviour of VICs. Particularly, hyperglycaemic conditions can reduce VIC interaction with and remodelling of the extracellular matrix. These results begin to link VIC metabolism and macroscopic behaviour such as cell–matrix interaction.

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Poggio, Paolo, Rachana Sainger, Juan B. Grau, Emanuela Branchetti, Eric Lai, Robert C. Gorman, Joseph H. Gorman III, Joseph E. Bavaria, Michael S. Sacks, and Giovanni Ferrari. "Biomechanical Activation of Human Valvular Interstitial Cells from Early Stage of CAVD." QScience Proceedings 2012, no. 4 (June 11, 2012): 67. http://dx.doi.org/10.5339/qproc.2012.heartvalve.4.67.

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Kekewska, Alexandra, Tilo Görnemann, Florian Jantschak, Erika Glusa, and Heinz H. Pertz. "Antiserotonergic Properties of Terguride in Blood Vessels, Platelets, and Valvular Interstitial Cells." Journal of Pharmacology and Experimental Therapeutics 340, no. 2 (November 2, 2011): 369–76. http://dx.doi.org/10.1124/jpet.111.187906.

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Porras, Ana M., Dhanansayan Shanmuganayagam, Jennifer J. Meudt, Christian G. Krueger, Jess D. Reed, and Kristyn S. Masters. "Gene expression profiling of valvular interstitial cells in Rapacz familial hypercholesterolemic swine." Genomics Data 2 (December 2014): 261–63. http://dx.doi.org/10.1016/j.gdata.2014.08.004.

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Masters, Kristyn S., Darshita N. Shah, Leslie A. Leinwand, and Kristi S. Anseth. "Crosslinked hyaluronan scaffolds as a biologically active carrier for valvular interstitial cells." Biomaterials 26, no. 15 (May 2005): 2517–25. http://dx.doi.org/10.1016/j.biomaterials.2004.07.018.

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Zhu, Enyi, Zihao Liu, Wanbing He, Bingqing Deng, Xiaorong Shu, Zhijian He, Xiaoying Wu, Xiao Ke, and Ruqiong Nie. "CC chemokine receptor 2 functions in osteoblastic transformation of valvular interstitial cells." Life Sciences 228 (July 2019): 72–84. http://dx.doi.org/10.1016/j.lfs.2019.04.050.

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McCoy, Chloe M., Dylan Q. Nicholas, and Kristyn S. Masters. "Sex-Related Differences in Gene Expression by Porcine Aortic Valvular Interstitial Cells." PLoS ONE 7, no. 7 (July 10, 2012): e39980. http://dx.doi.org/10.1371/journal.pone.0039980.

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43

Katwa, Laxmansa C., Suresh C. Tyagi, Scott E. Campbell, Soon Jin Lee, George T. Cicila, and Karl T. Weber. "Valvular interstitial cells express angiotensinogen and cathepsin D, and generate angiotensin peptides." International Journal of Biochemistry & Cell Biology 28, no. 7 (July 1996): 807–21. http://dx.doi.org/10.1016/1357-2725(96)00012-x.

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Roosens, Annelies, Mahtab Asadian, Nathalie De Geyter, Pamela Somers, and Ria Cornelissen. "Complete Static Repopulation of Decellularized Porcine Tissues for Heart Valve Engineering: An in vitro Study." Cells Tissues Organs 204, no. 5-6 (2017): 270–82. http://dx.doi.org/10.1159/000480660.

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To date, a completely in vitro repopulated tissue-engineered heart valve has not been developed. This study focused on sequentially seeding 2 cell populations onto porcine decellularized heart valve leaflets (HVL) and pericardia (PER) to obtain fully repopulated tissues. For repopulation of the interstitium, porcine valvular interstitial cells (VIC) and bone marrow-derived mesenchymal stem cells (BM-MSC) or adipose tissue-derived stem cells (ADSC) were used. In parallel, the culture medium was supplemented with ascorbic acid 2-phosphate (AA) and its effect on recolonization was investigated. Subsequently and in order to obtain an endothelial surface layer similar to those in native HVL, valvular endothelial cells (VEC) were seeded onto the scaffolds. It was shown that VIC efficiently recolonized HVL and partially also PER. On the other hand, stem cells only demonstrated limited or no subsurface cell infiltration of HVL and PER. Interestingly, the addition of AA increased the migratory capacity of both stem cell populations. However, this was more pronounced for BM-MSC, and recolonization of HVL appeared to be more efficient than that of PER tissue. VEC were demonstrated to generate a new endothelial layer on HVL and PER. However, scanning microscopy revealed that these endothelial cells were not allowed to fully spread onto PER. This study provided a proof of concept for the future generation of a bioactive tissue-engineered heart valve by showing that bioactive HVL could be generated in vitro within 14 days via complete repopulation of the interstitium with BM-MSC or VIC and subsequent generation of an entirely new endothelium.

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Brody, Sarah, Jillian McMahon, Li Yao, Margret O’Brien, Peter Dockery, and Abhay Pandit. "The effect of cholecyst-derived extracellular matrix on the phenotypic behaviour of valvular endothelial and valvular interstitial cells." Biomaterials 28, no. 8 (March 2007): 1461–69. http://dx.doi.org/10.1016/j.biomaterials.2006.11.030.

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Wang, Faye, Cindy Zhang, Jae Kwagh, Brian Strassle, Jinqing Li, Minxue Huang, Yunling Song, et al. "TGFβ2 and TGFβ3 mediate appropriate context-dependent phenotype of rat valvular interstitial cells." iScience 24, no. 3 (March 2021): 102133. http://dx.doi.org/10.1016/j.isci.2021.102133.

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Aize, Margaux, Harlyne Mpweme Bangando, Laura Brard, Nicolas Perzo, Romain Guinamard, and Christophe Simard. "Implication of TRPM4 ionic channel in osteogenic differentiation of human valvular interstitial cells." Archives of Cardiovascular Diseases Supplements 14, no. 2 (June 2022): 200. http://dx.doi.org/10.1016/j.acvdsp.2022.04.097.

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Gao, Yuan, Ning Li, Qing Xue, Xinli Fan, Xiaohong Liu, and Lin Han. "Basic fibroblast growth factor inhibits aortic valvular interstitial cells calcification via Notch1 pathway." Journal of Investigative Medicine 70, no. 4 (January 24, 2022): 907–13. http://dx.doi.org/10.1136/jim-2021-002132.

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Calcific aortic valve disease (CAVD) is an active pathological process mediated by abnormal activation and transdifferentiation of valvular interstitial cells (VICs). The present study aims to investigate the function and underlying mechanism of the basic fibroblast growth factor (BFGF) on osteogenic differentiation of VICs. Porcine VICs cultured with osteogenic induction medium are supplemented with or without BFGF. Morphology of VICs is identified by fluorescein isothiocyanate-labeled phalloidin, the cell viability is assessed by the cell counting kit-8 method, and protein and mRNA expression level of osteogenic differentiation markers, including Runx2, osteopontin, and Sp7, are verified by western blot analysis and quantitative real-time PCR, respectively. RNA sequencing is used to identify changes in gene profiles. Alizarin Red S staining is used to measure calcium deposition. The results demonstrate that the content of calcium deposition and the expression level of osteogenic markers are downregulated by supplementing BFGF. Notch1 signaling pathway is extracted as a candidate target after bioinformatics analysis by RNA sequencing. The transfection of si-Notch1 abolishes the calcification inhibitory effect of BFGF. Taken together, our findings shed the light on the mechanism and potential therapeutics of BFGF for CAVD.

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Wang, Xinmei, Nandini Deb, and Carla M. R. Lacerda. "Comparison of Serotonin-Regulated Calcific Processes in Aortic and Mitral Valvular Interstitial Cells." ACS Omega 6, no. 30 (July 20, 2021): 19494–505. http://dx.doi.org/10.1021/acsomega.1c01723.

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Carracedo, Miguel, Oscar Persson, Peter Saliba-Gustafsson, Gonzalo Artiach, Ewa Ehrenborg, Per Eriksson, Anders Franco-Cereceda, and Magnus Bäck. "Upregulated Autophagy in Calcific Aortic Valve Stenosis Confers Protection of Valvular Interstitial Cells." International Journal of Molecular Sciences 20, no. 6 (March 25, 2019): 1486. http://dx.doi.org/10.3390/ijms20061486.

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Autophagy serves as a cell survival mechanism which becomes dysregulated under pathological conditions and aging. Aortic valve thickening and calcification causing left ventricular outflow obstruction is known as calcific aortic valve stenosis (CAVS). CAVS is a chronic and progressive disease which increases in incidence and severity with age. Currently, no medical treatment exists for CAVS, and the role of autophagy in the disease remains largely unexplored. To further understand the role of autophagy in the progression of CAVS, we analyzed expression of key autophagy genes in healthy, thickened, and calcified valve tissue from 55 patients, and compared them with nine patients without significant CAVS, undergoing surgery for aortic regurgitation (AR). This revealed a upregulation in autophagy exclusively in the calcified tissue of CAVS patients. This difference in autophagy between CAVS and AR was explored by LC3 lipidation in valvular interstitial cells (VICs), revealing an upregulation in autophagic flux in CAVS patients. Inhibition of autophagy by bafilomycin-A1 led to a decrease in VIC survival. Finally, treatment of VICs with high phosphate led to an increase in autophagic activity. In conclusion, our data suggests that autophagy is upregulated in the calcified tissue of CAVS, serving as a compensatory and pro-survival mechanism.

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