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Article ; Online: Vascular stiffening and endothelial dysfunction in atherosclerosis.

Hooglugt, Aukie / Klatt, Olivia / Huveneers, Stephan

2022 Volume 33, Issue 6, Page(s) 353–363

Abstract: Purpose of review: Aging is an important risk factor for cardiovascular disease and is associated with increased vessel wall stiffness. Pathophysiological stiffening, notably in arteries, disturbs the integrity of the vascular endothelium and promotes ... ...

Abstract	Purpose of review: Aging is an important risk factor for cardiovascular disease and is associated with increased vessel wall stiffness. Pathophysiological stiffening, notably in arteries, disturbs the integrity of the vascular endothelium and promotes permeability and transmigration of immune cells, thereby driving the development of atherosclerosis and related vascular diseases. Effective therapeutic strategies for arterial stiffening are still lacking. Recent findings: Here, we overview the literature on age-related arterial stiffening, from patient-derived data to preclinical in-vivo and in-vitro findings. First, we overview the common techniques that are used to measure stiffness and discuss the observed stiffness values in atherosclerosis and aging. Next, the endothelial response to stiffening and possibilities to attenuate this response are discussed. Summary: Future research that will define the endothelial contribution to stiffness-related cardiovascular disease may provide new targets for intervention to restore endothelial function in atherosclerosis and complement the use of currently applied lipid-lowering, antihypertensive, and anti-inflammatory drugs.
MeSH term(s)	Humans ; Cardiovascular Diseases ; Vascular Stiffness/physiology ; Endothelium, Vascular/physiology ; Atherosclerosis ; Arteries
Language	English
Publishing date	2022-10-21
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1045394-5
ISSN	1473-6535 ; 0957-9672
ISSN (online)	1473-6535
ISSN	0957-9672
DOI	10.1097/MOL.0000000000000852
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Article ; Online: Opening the vascular gate.

Malinova, Tsveta S / Huveneers, Stephan

Nature nanotechnology

2019 Volume 14, Issue 3, Page(s) 195–196

MeSH term(s)	Breast Neoplasms ; Humans ; Ion Channel Gating ; Models, Molecular ; Nanoparticles
Language	English
Publishing date	2019-01-28
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2254964-X
ISSN	1748-3395 ; 1748-3387
ISSN (online)	1748-3395
ISSN	1748-3387
DOI	10.1038/s41565-019-0372-7
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Article ; Online: Vinculin strengthens the endothelial barrier during vascular development.

van der Stoel, Miesje M / Kotini, Maria P / Schoon, Rianne M / Affolter, Markus / Belting, Heinz-Georg / Huveneers, Stephan

Vascular biology (Bristol, England)

2023 Volume 5, Issue 1

Abstract: Remodelling of cell-cell junctions is crucial for proper tissue development and barrier function. The cadherin-based adherens junctions anchor via β-catenin and α-catenin to the actomyosin cytoskeleton, together forming a junctional mechanotransduction ... ...

Abstract	Remodelling of cell-cell junctions is crucial for proper tissue development and barrier function. The cadherin-based adherens junctions anchor via β-catenin and α-catenin to the actomyosin cytoskeleton, together forming a junctional mechanotransduction complex. Tension-induced conformational changes in the mechanosensitive α-catenin protein induce junctional vinculin recruitment. In endothelial cells, vinculin protects the remodelling of VE-cadherin junctions. In this study, we have addressed the role of vinculin in endothelial barrier function in the developing vasculature. In vitro experiments, using endothelial cells in which α-catenin was replaced by a vinculin-binding-deficient mutant, showed that junctional recruitment of vinculin promotes endothelial barrier function. To assess the role of vinculin within blood vessels in vivo, we next investigated barrier function in the vasculature of vcl knockout zebrafish. In the absence of vinculin, sprouting angiogenesis and vessel perfusion still occurred. Intriguingly, the absence of vinculin made the blood vessels more permeable for 10 kDa dextran molecules but not for larger tracers. Taken together, our findings demonstrate that vinculin strengthens the endothelial barrier and prevents vascular leakage in developing vessels.
Language	English
Publishing date	2023-01-27
Publishing country	England
Document type	Journal Article
ISSN	2516-5658
ISSN (online)	2516-5658
DOI	10.1530/VB-22-0012
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Article ; Online: Sensing of Cytoskeletal Forces by Asymmetric Adherens Junctions.

Malinova, Tsveta S / Huveneers, Stephan

Trends in cell biology

2017 Volume 28, Issue 4, Page(s) 328–341

Abstract: Within tissues, key cellular adaptations occur via mechanotransduction responses at cell-cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked ... ...

Abstract	Within tissues, key cellular adaptations occur via mechanotransduction responses at cell-cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked to the force-propagating and -generating actomyosin cytoskeleton. Recent studies have found that AJs maintain monolayer integrity in dynamic tissues and drive collective cell behavior by converting into asymmetric remodeling entities. Here, we overview the molecular processes that may explain how asymmetric cell-cell junctions sense differences in cytoskeletal geometry between cells. We discuss the link between cadherin-complex dynamics and the actomyosin cytoskeleton at asymmetric cell-cell junctions. We then outline the role of Bin/Amphiphysin/Rvs (BAR) proteins, cytoplasmic regulators of endocytosis and cytoskeletal dynamics that sense force-induced membrane curvature, at AJs undergoing asymmetric remodeling. Lastly, we highlight the physiological importance of junctional asymmetry for epithelial and vascular tissue and discuss its potential role in disease.
MeSH term(s)	Actomyosin/metabolism ; Adherens Junctions/metabolism ; Animals ; Cadherins/metabolism ; Cell Membrane/metabolism ; Cytoskeleton/metabolism ; Endocytosis/physiology ; Humans ; Mechanotransduction, Cellular/physiology ; Models, Biological
Chemical Substances	Cadherins ; Actomyosin (9013-26-7)
Language	English
Publishing date	2017-11-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2017.11.002
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Zs.A 3410: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: DLC1 promotes mechanotransductive feedback for YAP via RhoGAP-mediated focal adhesion turnover.

Hooglugt, Aukie / van der Stoel, Miesje M / Shapeti, Apeksha / Neep, Beau F / de Haan, Annett / van Oosterwyck, Hans / Boon, Reinier A / Huveneers, Stephan

Journal of cell science

2024 Volume 137, Issue 8

Abstract: Angiogenesis is a tightly controlled dynamic process demanding a delicate equilibrium between pro-angiogenic signals and factors that promote vascular stability. The spatiotemporal activation of the transcriptional co-factors YAP (herein referring to ... ...

Abstract	Angiogenesis is a tightly controlled dynamic process demanding a delicate equilibrium between pro-angiogenic signals and factors that promote vascular stability. The spatiotemporal activation of the transcriptional co-factors YAP (herein referring to YAP1) and TAZ (also known WWTR1), collectively denoted YAP/TAZ, is crucial to allow for efficient collective endothelial migration in angiogenesis. The focal adhesion protein deleted-in-liver-cancer-1 (DLC1) was recently described as a transcriptional downstream target of YAP/TAZ in endothelial cells. In this study, we uncover a negative feedback loop between DLC1 expression and YAP activity during collective migration and sprouting angiogenesis. In particular, our study demonstrates that signaling via the RhoGAP domain of DLC1 reduces nuclear localization of YAP and its transcriptional activity. Moreover, the RhoGAP activity of DLC1 is essential for YAP-mediated cellular processes, including the regulation of focal adhesion turnover, traction forces, and sprouting angiogenesis. We show that DLC1 restricts intracellular cytoskeletal tension by inhibiting Rho signaling at the basal adhesion plane, consequently reducing nuclear YAP localization. Collectively, these findings underscore the significance of DLC1 expression levels and its function in mitigating intracellular tension as a pivotal mechanotransductive feedback mechanism that finely tunes YAP activity throughout the process of sprouting angiogenesis.
MeSH term(s)	GTPase-Activating Proteins/metabolism ; GTPase-Activating Proteins/genetics ; Focal Adhesions/metabolism ; Focal Adhesions/genetics ; Humans ; Tumor Suppressor Proteins/metabolism ; Tumor Suppressor Proteins/genetics ; Mechanotransduction, Cellular ; Transcription Factors/metabolism ; Transcription Factors/genetics ; YAP-Signaling Proteins/metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Feedback, Physiological ; Animals ; Human Umbilical Vein Endothelial Cells/metabolism ; Cell Movement ; Neovascularization, Physiologic ; Cell Cycle Proteins/metabolism ; Cell Cycle Proteins/genetics ; Mice
Chemical Substances	GTPase-Activating Proteins ; DLC1 protein, human ; Tumor Suppressor Proteins ; Transcription Factors ; YAP-Signaling Proteins ; Adaptor Proteins, Signal Transducing ; rho GTPase-activating protein ; YAP1 protein, human ; Cell Cycle Proteins
Language	English
Publishing date	2024-04-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.261687
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Zs.A 1200: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 14: Show issues

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Article ; Online: Cell-cell junctional mechanotransduction in endothelial remodeling.

Dorland, Yvonne L / Huveneers, Stephan

Cellular and molecular life sciences : CMLS

2017 Volume 74, Issue 2, Page(s) 279–292

Abstract: The vasculature is one of the most dynamic tissues that encounter numerous mechanical cues derived from pulsatile blood flow, blood pressure, activity of smooth muscle cells in the vessel wall, and transmigration of immune cells. The inner layer of blood ...

Abstract	The vasculature is one of the most dynamic tissues that encounter numerous mechanical cues derived from pulsatile blood flow, blood pressure, activity of smooth muscle cells in the vessel wall, and transmigration of immune cells. The inner layer of blood and lymphatic vessels is covered by the endothelium, a monolayer of cells which separates blood from tissue, an important function that it fulfills even under the dynamic circumstances of the vascular microenvironment. In addition, remodeling of the endothelial barrier during angiogenesis and trafficking of immune cells is achieved by specific modulation of cell-cell adhesion structures between the endothelial cells. In recent years, there have been many new discoveries in the field of cellular mechanotransduction which controls the formation and destabilization of the vascular barrier. Force-induced adaptation at endothelial cell-cell adhesion structures is a crucial node in these processes that challenge the vascular barrier. One of the key examples of a force-induced molecular event is the recruitment of vinculin to the VE-cadherin complex upon pulling forces at cell-cell junctions. Here, we highlight recent advances in the current understanding of mechanotransduction responses at, and derived from, endothelial cell-cell junctions. We further discuss their importance for vascular barrier function and remodeling in development, inflammation, and vascular disease.
MeSH term(s)	Disease ; Endothelial Cells/metabolism ; Humans ; Intercellular Junctions/metabolism ; Mechanotransduction, Cellular ; Neovascularization, Physiologic ; Vascular Stiffness
Language	English
Publishing date	2017-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-016-2325-8
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Article ; Online: Cell-cell junctions as sensors and transducers of mechanical forces.

Angulo-Urarte, Ana / van der Wal, Tanne / Huveneers, Stephan

Biochimica et biophysica acta. Biomembranes

2020 Volume 1862, Issue 9, Page(s) 183316

Abstract: Epithelial and endothelial monolayers are multicellular sheets that form barriers between the 'outside' and 'inside' of tissues. Cell-cell junctions, made by adherens junctions, tight junctions and desmosomes, hold together these monolayers. They form ... ...

Abstract	Epithelial and endothelial monolayers are multicellular sheets that form barriers between the 'outside' and 'inside' of tissues. Cell-cell junctions, made by adherens junctions, tight junctions and desmosomes, hold together these monolayers. They form intercellular contacts by binding their receptor counterparts on neighboring cells and anchoring these structures intracellularly to the cytoskeleton. During tissue development, maintenance and pathogenesis, monolayers encounter a range of mechanical forces from the cells themselves and from external systemic forces, such as blood pressure or tissue stiffness. The molecular landscape of cell-cell junctions is diverse, containing transmembrane proteins that form intercellular bonds and a variety of cytoplasmic proteins that remodel the junctional connection to the cytoskeleton. Many junction-associated proteins participate in mechanotransduction cascades to confer mechanical cues into cellular responses that allow monolayers to maintain their structural integrity. We will discuss force-dependent junctional molecular events and their role in cell-cell contact organization and remodeling.
MeSH term(s)	Adherens Junctions/chemistry ; Adherens Junctions/genetics ; Blood Pressure/genetics ; Cytoskeleton/chemistry ; Desmosomes/chemistry ; Desmosomes/genetics ; Endothelial Cells/chemistry ; Epithelial Cells/chemistry ; Humans ; Intercellular Junctions/chemistry ; Intercellular Junctions/genetics ; Mechanical Phenomena ; Membrane Proteins/chemistry ; Membrane Proteins/genetics ; Tight Junctions/chemistry ; Tight Junctions/genetics
Chemical Substances	Membrane Proteins
Language	English
Publishing date	2020-04-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2642 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2642 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamem.2020.183316
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Article: Endothelial YAP/TAZ Signaling in Angiogenesis and Tumor Vasculature.

Hooglugt, Aukie / van der Stoel, Miesje M / Boon, Reinier A / Huveneers, Stephan

Frontiers in oncology

2021 Volume 10, Page(s) 612802

Abstract: Solid tumors are dependent on vascularization for their growth. The hypoxic, stiff, and pro-angiogenic tumor microenvironment induces angiogenesis, giving rise to an immature, proliferative, and permeable vasculature. The tumor vessels promote tumor ... ...

Abstract	Solid tumors are dependent on vascularization for their growth. The hypoxic, stiff, and pro-angiogenic tumor microenvironment induces angiogenesis, giving rise to an immature, proliferative, and permeable vasculature. The tumor vessels promote tumor metastasis and complicate delivery of anti-cancer therapies. In many types of tumors, YAP/TAZ activation is correlated with increased levels of angiogenesis. In addition, endothelial YAP/TAZ activation is important for the formation of new blood and lymphatic vessels during development. Oncogenic activation of YAP/TAZ in tumor cell growth and invasion has been studied in great detail, however the role of YAP/TAZ within the tumor endothelium remains insufficiently understood, which complicates therapeutic strategies aimed at targeting YAP/TAZ in cancer. Here, we overview the upstream signals from the tumor microenvironment that control endothelial YAP/TAZ activation and explore the role of their downstream targets in driving tumor angiogenesis. We further discuss the potential for anti-cancer treatments and vascular normalization strategies to improve tumor therapies.
Language	English
Publishing date	2021-02-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2020.612802
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Article: Editorial: Endothelial Dynamics in Health and Disease.

Jones, Elizabeth A V / Graupera, Mariona / van Buul, Jaap D / Huveneers, Stephan

Frontiers in physiology

2020 Volume 11, Page(s) 611117

Language	English
Publishing date	2020-11-19
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2020.611117
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Article ; Online: Endothelial dysfunction in Marfan syndrome mice is restored by resveratrol.

Mieremet, Arnout / van der Stoel, Miesje / Li, Siyu / Coskun, Evrim / van Krimpen, Tsveta / Huveneers, Stephan / de Waard, Vivian

Scientific reports

2022 Volume 12, Issue 1, Page(s) 22504

Abstract: Patients with Marfan syndrome (MFS) develop thoracic aortic aneurysms as the aorta presents excessive elastin breaks, fibrosis, and vascular smooth muscle cell (vSMC) death due to mutations in the FBN1 gene. Despite elaborate vSMC to aortic endothelial ... ...

Abstract	Patients with Marfan syndrome (MFS) develop thoracic aortic aneurysms as the aorta presents excessive elastin breaks, fibrosis, and vascular smooth muscle cell (vSMC) death due to mutations in the FBN1 gene. Despite elaborate vSMC to aortic endothelial cell (EC) signaling, the contribution of ECs to the development of aortic pathology remains largely unresolved. The aim of this study is to investigate the EC properties in Fbn1
MeSH term(s)	Mice ; Animals ; Aortic Aneurysm/metabolism ; Resveratrol/pharmacology ; Resveratrol/metabolism ; Marfan Syndrome/genetics ; Aorta/metabolism ; Aortic Diseases/metabolism ; Fibrillin-1/genetics ; Fibrillin-1/metabolism
Chemical Substances	Resveratrol (Q369O8926L) ; Fibrillin-1
Language	English
Publishing date	2022-12-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-26662-5
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