CD117-positive cells and mast cells in adult human cardiac valves—observations and implications for the creation of bioengineered grafts

Veinot, John P.; Prichett-Pejic, Wendy; Song, Junhui; Waghray, Geeta; Parks, William; Mesana, Thierry G.; Ruel, Marc

doi:10.1016/j.carpath.2005.08.005

Cited by 22 publications

(17 citation statements)

References 13 publications

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“…It was demonstrated on human cardiac samples that while the mast cells co-express c-kit and CD45, the c-kit+ CD45-cells express mRNA of the endothelial lineage [Sandstedt et al, 2010]. Almost all the c-kit+ cells in the cardiac valves are mast cells [Veinot et al, 2006]; therefore, the molecular identification of TCs in cardiac valves based on the expression of CD34, vimentin, PDGFRβ, and c-kit [Yang et al, 2014], but without using the mast cell tryptase or the CD45 marker, would not convince.…”

Section: Expression Of Stem/progenitor Markers In Cardiac Tcs: the Vamentioning

confidence: 99%

Myocardial Telocyte-Like Cells: A Review Including New Evidence

Iancu

Rusu

Mogoantă

et al. 2018

Cells Tissues Organs

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Telocytes (TCs) are a controversial cell type characterized by the presence of a particular kind of prolongations, known as telopodes, which are long, thin, and moniliform. A number of attempts has been made to establish the molecular phenotype of cardiac TCs (i.e., expression of c-kit, CD34, vimentin, PDGRFα, PDGRFβ, etc.). We designed an immunohistochemical study involving cardiac tissue samples obtained from 10 cadavers with the aim of determining whether there are TC-like interstitial cells that populate the interstitial space other than the mural microvascular cells. We applied the markers for CD31, CD34, PDGRFα, CD117/c-kit, and α-smooth muscle actin (α-SMA). We found that, in relation to two-dimensional cuts, the endothelial tubes could be misidentified as TC-like cells, the difference being the positive identification of endothelial lumina. Moreover, we found that cardiac pericytes express PDGRFα, CD117/c-kit, and α-SMA, and that they could also be misidentified as TCs when using light microscopy. We reviewed the respective values of the previously identified markers for achieving a clear-cut identification of cardiac TCs, highlighting the critical lack of specificity.

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Section: Expression Of Stem/progenitor Markers In Cardiac Tcs: the Vamentioning

confidence: 99%

Myocardial Telocyte-Like Cells: A Review Including New Evidence

Iancu

Rusu

Mogoantă

et al. 2018

Cells Tissues Organs

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“…14 That valve progenitors exist and contribute to cell regeneration or repair in adult valves has been speculated on 15 ; however, only recently has experimental evidence for valve progenitors been reported. 16,17 Indeed, bone marrow transplantation experiments in mice have shown that clonal hematopoietic stem cells engrafted into the aortic, pulmonary, and atrioventricular valves can differentiate into fibroblastlike cells. 18 In the course of our studies on the endothelium of postnatal valves, we identified clonal populations from human pulmonary valve leaflets with progenitor-like properties, demonstrated by their ability to differentiate into endothelial cells in response to VEGF or into myofibroblasts/smooth muscle cells (SMCs), reminiscent of valve interstitial cells, in response to TGF␤ 2 .…”

mentioning

confidence: 99%

Human Pulmonary Valve Progenitor Cells Exhibit Endothelial/Mesenchymal Plasticity in Response to Vascular Endothelial Growth Factor-A and Transforming Growth Factor-β ₂

Paruchuri

Yang

Aikawa

et al. 2006

Circulation Research

138

135

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Abstract-In situ analysis of fetal semilunar valve leaflets has revealed cells coexpressing endothelial and mesenchymal markers along the endothelium, with diminished frequency seen in adult valves. To determine whether such cells are progenitor cells, we isolated clonal populations from human pulmonary valves. The clones expressed endothelial markers but showed potential to further differentiate into endothelium in response to vascular endothelial growth factor (VEGF)-A. When exposed to transforming growth factor (TGF)-␤ 2 , individual clones adopted a mesenchymal phenotype to varying degrees and expressed markers of endothelial to mesenchymal transformation (EMT). Both VEGF-and TGF␤ 2 -induced phenotypic changes were partially reversible, indicating the plasticity of these cells. When challenged with VEGF or TGF␤ 2 , a hierarchy of endothelial/mesenchymal potential could be seen among the clonal populations: cells initially closer to an endothelial phenotype showed a strong response to TGF␤ 2 that could be inhibited by VEGF, whereas cells closer to a mesenchymal phenotype responded to TGF␤ 2 but were resistant to endothelialinducing effects of VEGF. These findings suggest the presence of bipotential valve progenitor cells with ability to differentiate into either endothelial or interstitial cells of the valve leaflet. Understanding the differentiation potential and function of these cells may be important for understanding heart valve disease and may also be applied to current paradigms for creating tissue-engineered heart valves. Key Words: cell culture Ⅲ endothelial cell differentiation Ⅲ endothelial cells Ⅲ heart valves Ⅲ progenitor cells Ⅲ transdifferentiation Ⅲ vascular endothelial growth factor Ⅲ vascular endothelium V alvular heart disease is a major cause of morbidity, often resulting in the need to replace the valve with a mechanical or bioprosthetic valve. There is a pressing need for improved approaches, especially for children because calcification and destruction of the replacement valve occurs more rapidly in children and young adults. 1 Possible strategies include stimulating endogenous repair pathways or using autologous progenitor cells to create tissue-engineered heart valves that will grow with the child. For both approaches, an increased understanding of mechanisms underlying the normal cellular turnover and repair throughout adult life will be essential.During embryonic valve development, a subset of endocardial endothelial cells, driven by signals from the underlying myocardium, change their phenotype to mesenchymal cells and migrate into the cardiac jelly to form endocardial cushions, the primordial of valves and cardiac septa of the adult heart. 2 This transdifferentiation of endocardial cells to mesenchymal cells and migration away from the endothelial layer is termed endothelial-mesenchymal transformation (EMT). Studies from Markwald and coworkers show that during EMT, the activated endothelial cells lose cell-cell contacts, gain mesenchymal markers such as ␣-smooth muscle actin (␣-SM...

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“…Veinot et al analyzed five valves with MD and observed an increase in markers of mast cells (CD117), suggesting the participation of an inflammatory process triggered by myxoid degeneration. CD117 + cells are young cells identified in mitral valves that represent a degree of heart regeneration capacity against stress, trauma or ischemia [3]. Barth et al analyzed the presence of CD34 + fibrocytes in 15 myxoid valves and 10 valves without degeneration and found that these cells appear to be morphologically altered [7].…”

Section: Discussionmentioning

confidence: 99%

“…It occurs when the valve matrix is compromised due to an imbalance in the levels of acid mucopolysaccharides [2, 3]. Mitral valve prolapse is initiated by MVD, which serves as an anatomical substrate affecting the valve matrix.…”

Section: Introductionmentioning

confidence: 99%

Infectious agents is a risk factor for myxomatous mitral valve degeneration: A case control study

et al. 2017

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Background: The etiology of myxomatous mitral valve degeneration (MVD) is not fully understood and may depend on time or environmental factors for which the interaction of infectious agents has not been documented. The purpose of the study is to analyze the effect of Mycoplasma pneumoniae (Mp), Chlamydophila pneumoniae (Cp) and Borrelia burgdorferi (Bb) on myxomatous mitral valve degeneration pathogenesis and establish whether increased in inflammation and collagen degradation in myxomatous mitral valve degeneration etiopathogenesis. Methods: An immunohistochemical test was performed to detect the inflammatory cells (CD20, CD45, CD68) and Mp, Bb and MMP9 antigens in two groups. The in situ hybridization was performed to detect Chlamydophila pneumoniae and the bacteria study was performed using transmission electron microscopy. Group 1 (n = 20), surgical specimen composed by myxomatous mitral valve degeneration, and group 2 (n = 20), autopsy specimen composed by normal mitral valve. The data were analyzed using SigmaStat version 20 (SPSS Inc., Chicago, IL, USA). The groups were compared using Student's t test, Mann-Whitney test. A correlation analysis was performed using Spearman's correlation test. P values lower than 0.05 were considered statistically significant.

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CD117-positive cells and mast cells in adult human cardiac valves—observations and implications for the creation of bioengineered grafts

Cited by 22 publications

References 13 publications

Myocardial Telocyte-Like Cells: A Review Including New Evidence

Myocardial Telocyte-Like Cells: A Review Including New Evidence

Human Pulmonary Valve Progenitor Cells Exhibit Endothelial/Mesenchymal Plasticity in Response to Vascular Endothelial Growth Factor-A and Transforming Growth Factor-β ₂

Infectious agents is a risk factor for myxomatous mitral valve degeneration: A case control study

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CD117-positive cells and mast cells in adult human cardiac valves—observations and implications for the creation of bioengineered grafts

Cited by 22 publications

References 13 publications

Myocardial Telocyte-Like Cells: A Review Including New Evidence

Myocardial Telocyte-Like Cells: A Review Including New Evidence

Human Pulmonary Valve Progenitor Cells Exhibit Endothelial/Mesenchymal Plasticity in Response to Vascular Endothelial Growth Factor-A and Transforming Growth Factor-β 2

Infectious agents is a risk factor for myxomatous mitral valve degeneration: A case control study

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Human Pulmonary Valve Progenitor Cells Exhibit Endothelial/Mesenchymal Plasticity in Response to Vascular Endothelial Growth Factor-A and Transforming Growth Factor-β ₂