Regulation of Partial and Reversible Endothelial-to-Mesenchymal Transition in Angiogenesis

Fang, Jennifer S.; Hultgren, Nan W.; Hughes, Christopher C.W.

doi:10.3389/fcell.2021.702021

Cited by 29 publications

(49 citation statements)

References 143 publications

(238 reference statements)

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“…EndMT leads to alteration of gene expression: cells lose their endothelial markers (CDH1, CDH5, PECAM1, TIE1, TEK, VWF, OCLN, CLDN5, TJP1) and obtain mesenchymal ones (CDH2,CDH13, ACTA2, VIM, S100A4, PLAU, PLAUR, MMP14, FN1, COL1A1) [ 13 , 14 ] ( Figure 3 a).…”

Section: Resultsmentioning

confidence: 99%

New Insight on 2D In Vitro Angiogenesis Models: All That Stretches Is Not a Tube

Белоглазова

Zubkova

Дергилев

et al. 2022

Cells

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A Matrigel-based tube formation assay is a simple and widely accepted 2D angiogenesis model in vitro. Extracellular matrix (EM) proteins and growth factors (GFs) from MatrigelTM exclusively trigger endothelial cell (EC) tubular network (ETN) formation. Co-culture of ECs with mesenchymal stromal cells (MSCs) is another and more reliable in vitro angiogenesis assay. MSCs modulate ETN formation through intercellular interactions and as a supplier of EM and GFs. The aim of the present study was to compare the expression profile of ECs in both models. We revealed upregulation of the uPA, uPAR, Jagged1, and Notch2 genes in dividing/migrating ECs and for ECs in both experimental models at 19 h. The expression of endothelial–mesenchymal transition genes largely increased in co-cultured ECs whereas Notch and Hippo signaling pathway genes were upregulated in ECs on MatrigelTM. We showed that in the co-culture model, basement membrane (BM) deposition is limited only to cell-to-cell contacts in contrast to MatrigelTM, which represents by itself fully pre-assembled BM matrix. We suggest that ETN in a co-culture model is still in a dynamic process due to immature BM whereas ECs in the MatrigelTM assay seem to be at the final stage of ETN formation.

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Section: Resultsmentioning

confidence: 99%

New Insight on 2D In Vitro Angiogenesis Models: All That Stretches Is Not a Tube

Белоглазова

Zubkova

Дергилев

et al. 2022

Cells

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“…28,47 As suggested by 2 review articles, partial EndoMT may be closely linked to angiogenesis. 47,206 During angiogenesis, tip cells undergo distinct morphological and functional changes, which also occur during EndoMT. They de novo express mesenchymal markers, undergo similar cytoskeletal rearrangements, and express MMPs for breakdown of the basal membrane.…”

Section: Partial Vs Full Endomtmentioning

confidence: 99%

“…47 Of note, common plasticity events during angiogenic sprouting and EndoMT seem to also share similar signaling pathways, which are largely controlled by the transcription factors Slug and Snail, respectively. 47,206 However, tip cells largely retain EC marker expression. 206,207 Importantly, they maintain CD31 and thus cell-cell connections with stalk cells, when migrating in a connected "train" during the formation of an emerging vessel sprout.…”

Section: Partial Vs Full Endomtmentioning

confidence: 99%

“…47,206 However, tip cells largely retain EC marker expression. 206,207 Importantly, they maintain CD31 and thus cell-cell connections with stalk cells, when migrating in a connected "train" during the formation of an emerging vessel sprout. 206 In contrast, loss of cell-cell contacts and migration of individual cells away from the capillary bed, are key events during full EndoMT.…”

Section: Partial Vs Full Endomtmentioning

confidence: 99%

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Endothelial cell plasticity in kidney fibrosis and disease

Pohl,

Schiessl

2023

Acta Physiologica

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Renal endothelial cells demonstrate an impressive remodeling potential during angiogenic sprouting, vessel repair or while transitioning into mesenchymal cells. These different processes may play important roles in both renal disease progression or regeneration while underlying signaling pathways of different endothelial cell plasticity routes partly overlap. Angiogenesis contributes to wound healing after kidney injury and pharmaceutical modulation of angiogenesis may home a great therapeutic potential. Yet, it is not clear whether any differentiated endothelial cell can proliferate or whether regenerative processes are largely controlled by resident or circulating endothelial progenitor cells. In the glomerular compartment for example, a distinct endothelial progenitor cell population may remodel the glomerular endothelium after injury. Endothelial‐to‐mesenchymal transition (EndoMT) in the kidney is vastly documented and often associated with endothelial dysfunction, fibrosis, and kidney disease progression. Especially the role of EndoMT in renal fibrosis is controversial. Studies on EndoMT in vivo determined possible conclusions on the pathophysiological role of EndoMT in the kidney, but whether endothelial cells really contribute to kidney fibrosis and if not what other cellular and functional outcomes derive from EndoMT in kidney disease is unclear. Sequencing data, however, suggest no participation of endothelial cells in extracellular matrix deposition. Thus, more in‐depth classification of cellular markers and the fate of EndoMT cells in the kidney is needed. In this review, we describe different signaling pathways of endothelial plasticity, outline methodological approaches and evidence for functional and structural implications of angiogenesis and EndoMT in the kidney, and eventually discuss controversial aspects in the literature.

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“…ECs involve a progressive transition to mesenchymal via a fluid spectrum of intermediate cell states called partial EndoMT, which enables the temporary and reversible adoption of a hybrid endothelial-mesenchymal cell state [ 108 ]. This might may be triggered by signaling cross-talk regulatory mechanisms that limit complete progression through the EndoMT, preventing excessive mesenchymal transition.…”

Section: Partial and Reversible Endomtmentioning

confidence: 99%

The Role of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease

Peng

Shan

Cui

et al. 2022

Cells

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Endothelial-to-mesenchymal transition (EndoMT) is the process of endothelial cells progressively losing endothelial-specific markers and gaining mesenchymal phenotypes. In the normal physiological condition, EndoMT plays a fundamental role in forming the cardiac valves of the developing heart. However, EndoMT contributes to the development of various cardiovascular diseases (CVD), such as atherosclerosis, valve diseases, fibrosis, and pulmonary arterial hypertension (PAH). Therefore, a deeper understanding of the cellular and molecular mechanisms underlying EndoMT in CVD should provide urgently needed insights into reversing this condition. This review summarizes a 30-year span of relevant literature, delineating the EndoMT process in particular, key signaling pathways, and the underlying regulatory networks involved in CVD.

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Regulation of Partial and Reversible Endothelial-to-Mesenchymal Transition in Angiogenesis

Cited by 29 publications

References 143 publications

New Insight on 2D In Vitro Angiogenesis Models: All That Stretches Is Not a Tube

New Insight on 2D In Vitro Angiogenesis Models: All That Stretches Is Not a Tube

Endothelial cell plasticity in kidney fibrosis and disease

The Role of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease

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