Vascular changes in maturing granulation tissue

Sarkisov, D. S.; Kolokol'chikova, E. G.; Kaem, R. I.; Pal'tsyn, A. A.

doi:10.1007/bf00841219

Cited by 9 publications

(6 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to the studies described above, there is evidence to suggest that EndMT may occur in many other disease settings, such as chronic pulmonary hypertension (Zhu et al, 2006;Arciniegas et al, 2007), atherosclerosis (Mironov et al, 1995), wound healing (Sarkisov et al, 1988;Lee and Kay, 2006), and in both acute and chronic kidney injury (Zeisberg et al, 2008). These emerging reports have characterised EndMT primarily in terms of marker expression, but have not addressed the precise molecular mechanisms of EndMT in disease.…”

Section: Endothelial-to-mesenchymal Transition In Cardiac Fibrosis Anmentioning

confidence: 99%

The role of endothelial-to-mesenchymal transition in cancer progression

2008

View full text Add to dashboard Cite

Recent evidence has demonstrated that endothelial-to-mesenchymal transition (EndMT) may have a significant role in a number of diseases. Although EndMT has been previously studied as a critical process in heart development, it is now clear that EndMT can also occur postnatally in various pathologic settings, including cancer and cardiac fibrosis. During EndMT, resident endothelial cells delaminate from an organised cell layer and acquire a mesenchymal phenotype characterised by loss of cell–cell junctions, loss of endothelial markers, gain of mesenchymal markers, and acquisition of invasive and migratory properties. Endothelial-to-mesenchymal transition -derived cells are believed to function as fibroblasts in damaged tissue, and may therefore have an important role in tissue remodelling and fibrosis. In tumours, EndMT is an important source of cancer-associated fibroblasts (CAFs), which are known to facilitate tumour progression in several ways. These new findings suggest that targeting EndMT may be a novel therapeutic strategy, which is broadly applicable not only to cancer but also to various other disease states.

show abstract

Section: Endothelial-to-mesenchymal Transition In Cardiac Fibrosis Anmentioning

confidence: 99%

The role of endothelial-to-mesenchymal transition in cancer progression

2008

View full text Add to dashboard Cite

show abstract

“…One additional source of activated myofibroblast‐like cells is endothelial to mesenchymal transformation (EndMT), which is the transdifferentiation of endothelial cells to mesenchymal cells. EndMT was first observed in embryonic heart valve development, but more recent studies have shown that mesenchymal transformation can also occur in tissue homeostasis, such as wound healing, and in adult pathologies including cancer, cardiac fibrosis, and CAVD . EndMT has been observed near calcified nodules in human valves, and factors present in aortic valve disease including inflammatory cytokines (TGF‐β1, TNF‐α), pathological cyclic strain, and altered shear stress have individually been shown to induce this cell transformation in vitro in adult aortic VEC.…”

Section: Introductionmentioning

confidence: 99%

“…EndMT was first observed in embryonic heart valve development, 20 but more recent studies have shown that mesenchymal transformation can also occur in tissue homeostasis, such as wound healing, and in adult pathologies including cancer, cardiac fibrosis, and CAVD. [21][22][23][24][25][26][27] EndMT has been observed near calcified nodules in human valves, 26 and factors present in aortic valve disease including inflammatory cytokines (TGF-b1, TNF-a), 26,28 pathological cyclic strain, 29 and altered shear stress 30 have individually been shown to induce this cell transformation in vitro in adult aortic VEC. The process of EndMT begins when a subset of endothelial cells delaminate from the cell layer and lose cell-cell contacts, lose endothelial markers such as PECAM1 or VE-cadherin, gain mesenchymal markers like a-smooth muscle actin (a-SMA), and gain invasive and migratory properties.…”

Section: Introductionmentioning

confidence: 99%

Endothelial to mesenchymal transformation is induced by altered extracellular matrix in aortic valve endothelial cells

Dahal

Huang

Murray

et al. 2017

J Biomedical Materials Res

View full text Add to dashboard Cite

Alterations in shear stress, mechanical deformation, extracellular matrix (ECM) composition and exposure to inflammatory conditions are known to cause endothelial to mesenchymal transformation (EndMT). This change in endothelial phenotype has only recently been linked to adult pathologies such as cancer progression, organ fibrosis, and calcific aortic valve disease; and its function in adult physiology, especially in response to tissue mechanics, has not been rigorously investigated. EndMT is a response to mechanical and biochemical signals that results in the remodeling of underlying tissues. In diseased aortic valves, glycosaminoglycans (GAGs) are present in the collagen-rich valve fibrosa, and are deposited near calcified nodules. In this study, in vitro models of early and late-stage valve disease were developed by incorporating the GAGs chondroitin sulfate (CS), hyaluronic acid, and dermatan sulfate into 3D collagen hydrogels with or without exposure to TGF-β1 to simulate EndMT in response to microenvironmental changes. High levels of CS induced the highest rate of EndMT and led to the most collagen I and GAG production by mesenchymally transformed cells, which indicates a cell phenotype most likely to promote fibrotic disease. Mesenchymal transformation due to altered ECM was found to depend on cell-ECM bond strength and extracellular signal-regulated protein kinases 1/2 signaling. Determining the environmental conditions that induce and promote EndMT, and the subsequent behavior of mesenchymally transformed cells, will advance understanding on the role of endothelial cells in tissue regeneration or disease progression. © 2017 Wiley Periodicals Inc. J Biomed Mater Res Part A: 105A: 2729-2741, 2017.

show abstract

“…Morphological studies in human embryos suggest that endothelial-like cells may give rise to SMC during the maturation of both pulmonary arteries and veins (35,36). Findings in experimental wound repair have suggested that EnMT may also take place in the adult, reporting that capillary endothelial cells could undergo conversion into interstitial connective tissue mesenchymal-like cells in granulation tissue (85). Others have observed that microvascular endothelial cells transitioned into mesenchymal cells in response to chronic inflammatory stimuli (56,83).…”

mentioning

confidence: 96%

Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension

Arciniegas¹,

Frid²,

Douglas³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

308

277

View full text Add to dashboard Cite

All forms of pulmonary hypertension are characterized by structural changes in pulmonary arteries. Increased numbers of cells expressing alpha-smooth muscle (alpha-SM) actin is a nearly universal finding in the remodeled artery. Traditionally, it was assumed that resident smooth muscle cells were the exclusive source of these newly appearing alpha-SM actin-expressing cells. However, rapidly emerging experimental evidence suggests other, alternative cellular sources of these cells. One possibility is that endothelial cells can transition into mesenchymal cells expressing alpha-SM actin and that this process contributes to the accumulation of SM-like cells in vascular pathologies. We review the evidence that endothelial-mesenchymal transition is an important contributor to cardiac and vascular development as well as to pathophysiological vascular remodeling. Recent work has provided evidence for the role of transforming growth factor-beta, Wnt, and Notch signaling in this process. The potential roles of matrix metalloproteinases and serine proteases are also discussed. Importantly, endothelial-mesenchymal transition may be reversible. Thus insights into the mechanisms controlling endothelial-mesenchymal transition are relevant to vascular remodeling and are important as we consider new therapies aimed at reversing pulmonary vascular remodeling.

show abstract

Vascular changes in maturing granulation tissue

Cited by 9 publications

References 3 publications

The role of endothelial-to-mesenchymal transition in cancer progression

The role of endothelial-to-mesenchymal transition in cancer progression

Endothelial to mesenchymal transformation is induced by altered extracellular matrix in aortic valve endothelial cells

Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension

Contact Info

Product

Resources

About